emedicine.medscape.com

Osteoarthritis 
Updated: Mar 19, 2019
Author: Carlos J Lozada, MD; Chief Editor: Herbert S Diamond, MD 

Overview

Practice Essentials
Osteoarthritis (see the image below) is the most common type of joint disease, affecting more than 30 million individuals in the
United States alone.[1] It is the leading cause of chronic disability in older adults, costing the US greater than $185 billion
annually.[2] It can be thought of as a degenerative disorder arising from the biochemical breakdown of articular (hyaline)
cartilage in the synovial joints. However, the current view holds that osteoarthritis involves not only the articular cartilage but the
entire joint organ, including the subchondral bone and synovium. (See the image below.)

Anteroposterior (AP) radiograph of the hip reveals severe superior migration of the femoral head (which reflects loss of
articular cartilage), subchondral sclerosis, prominent osteophytes, and a large Egger cyst in the superior acetabulum. Mild
flattening of the superior aspect of the femoral head is present.

Signs and symptoms

Symptoms of osteoarthritis include the following:

Deep, achy joint pain exacerbated by extensive use - The disease’s primary symptom

Reduced range of motion and crepitus - Frequently present

Stiffness during rest (gelling) - May develop, with morning joint stiffness usually lasting for less than 30 minutes

Osteoarthritis of the hand

Distal interphalangeal (DIP) joints are most often affected

 Proximal interphalangeal (PIP) joints and the carpometacarpal (cmc) joints at the base of the thumb are also typically
involved

Heberden nodes, which represent palpable osteophytes in the DIP joints, are more characteristic in women than in men

Inflammatory changes are typically absent, less pronounced, or go unnoticed

See Clinical Presentation for more detail.

Diagnosis

Osteoarthritis is typically diagnosed on the basis of clinical and radiographic evidence.[3, 4, 5, 6, 7] No specific laboratory
abnormalities are associated with osteoarthritis.

Imaging studies

Plain radiography - The imaging method of choice because radiographs are cost-effective and can be readily and quickly
obtained[5, 8] ; in the load-bearing areas, radiographs can depict joint-space loss, as well as subchondral bony sclerosis
and cyst formation

Computed tomography (CT) scanning - Rarely used in the diagnosis of primary osteoarthritis; however, it may be used in
the diagnosis of malalignment of the patellofemoral joint or of the foot and ankle joints

Magnetic resonance imaging (MRI) - Not necessary in most patients with osteoarthritis unless additional pathology
amenable to surgical repair is suspected; unlike radiography, MRI can directly visualize articular cartilage and other joint
tissues (eg, meniscus, tendon, muscle, or effusion)

Ultrasonography - No role in the routine clinical assessment of patients with osteoarthritis; however, it is being
investigated as a tool for monitoring cartilage degeneration, and it can be used for guided injections of joints not easily
accessed without imaging

Bone scanning - May be helpful in the early diagnosis of osteoarthritis of the hand[9] ; bone scans also can help
differentiate osteoarthritis from osteomyelitis, bone metastases, and metabolic bone diseases

Arthrocentesis

The presence of noninflammatory joint fluid helps distinguish osteoarthritis from other causes of joint pain. Other synovial fluid
findings that aid in the differentiation of osteoarthritis from other conditions are negative Gram stains and cultures, as well as
the absence of crystals when fluid is viewed under a polarized microscope.

See Workup for more detail.

Management

Nonpharmacologic interventions

The cornerstones of osteoarthritis therapy, nonpharmacologic interventions include the following:

Patient education

Heat and cold

Weight loss[10]

Exercise

Physical therapy

Occupational therapy

Unloading in certain joints (eg, knee and hip)

Pharmacologic therapy

For hand osteoarthritis, the American College of Rheumatology (ACR) conditionally recommends using one or more of the
following:

Topical capsaicin
 Topical nonsteroidal anti-inflammatory drugs (NSAIDs) - Including trolamine salicylate

Oral NSAIDs

Tramadol

For knee osteoarthritis, the ACR conditionally recommends using one of the following:

Acetaminophen

Oral NSAIDs

Topical NSAIDs

Tramadol

Intra-articular corticosteroid injections

For hip osteoarthritis, the ACR conditionally recommends using 1 or more of the following for initial management:

Acetaminophen

Oral NSAIDs

Tramadol

Intra-articular corticosteroid injections

Surgery

A referral to an orthopedic surgeon may be necessary if the osteoarthritis fails to respond to a medical management plan.
Surgical procedures for osteoarthritis include the following:

Arthroscopy

Osteotomy

Arthroplasty - Particularly with knee or hip osteoarthritis

Fusion

See Treatment and Medication for more detail.

Background
Osteoarthritis is the most common type of joint disease, affecting more than 30 million individuals in the United States alone
(see Epidemiology). It represents a heterogeneous group of conditions resulting in common histopathologic and radiologic
changes. It has been thought of as a degenerative disorder arising from biochemical breakdown of articular (hyaline) cartilage in
the synovial joints. However, the current view holds that osteoarthritis involves not only the articular cartilage but also the entire
joint organ, including the subchondral bone and synovium.

Osteoarthritis predominantly involves the weight-bearing joints, including the knees, hips, cervical and lumbosacral spine, and
feet. Other commonly affected joints include the distal interphalangeal (DIP), proximal interphalangeal (PIP), and
carpometacarpal (CMC) joints. This article primarily focuses on osteoarthritis of the hand, knee, and hip joints (see
Pathophysiology). For more information on arthritis in other joints, see Glenohumeral Arthritis and Wrist Arthritis.

Although osteoarthritis was previously thought to be caused largely by excessive wear and tear, increasing evidence points to
the contributions of abnormal mechanics and inflammation. In addition, some invasive procedures (eg, arthroscopic
meniscectomy) can result in rapid progression to osteoarthritis in the knee joint.[11] Therefore, the term degenerative joint
disease is no longer appropriate in referring to osteoarthritis. (See Pathophysiology.)

Historically, osteoarthritis has been divided into primary and secondary forms, though this division is somewhat artificial.
Secondary osteoarthritis is conceptually easier to understand: It refers to disease of the synovial joints that results from some
predisposing condition that has adversely altered the joint tissues (eg, trauma to articular cartilage or subchondral bone).
Secondary osteoarthritis can occur in relatively young individuals (see Etiology).[12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22]

The definition of primary osteoarthritis is more nebulous. Although this form of osteoarthritis is related to the aging process and
typically occurs in older individuals, it is, in the broadest sense of the term, an idiopathic phenomenon, occurring in previously
intact joints and having no apparent initiating factor.

Some clinicians limit the term primary osteoarthritis to the joints of the hands (specifically, the DIP and PIP joints and the joints
at the base of the thumb). Others include the knees, hips, and spine (apophyseal articulations) as well.

As underlying causes of osteoarthritis are discovered, the term primary, or idiopathic, osteoarthritis may become obsolete. For
instance, many investigators believe that most cases of primary osteoarthritis of the hip may, in fact, be due to subtle or even
unrecognizable congenital or developmental defects.

No specific laboratory abnormalities are associated with osteoarthritis. Rather, it is typically diagnosed on the basis of clinical
findings, with or without radiographic studies (see Workup).

The goals of osteoarthritis treatment include pain alleviation and improvement of functional status. Nonpharmacologic
interventions are the cornerstones of osteoarthritis therapy and include the following:

Patient education

Application of heat and cold

Weight loss

Exercise

Physical therapy

Occupational therapy

Joint unloading, in certain joints (eg, knee and hip)

Intra-articular pharmacologic therapy includes corticosteroid injection and viscosupplementation, which may provide pain relief
and have an anti-inflammatory effect on the affected joint. (See Treatment.) Oral pharmacologic therapy begins with
acetaminophen for mild or moderate pain without apparent inflammation.

If the clinical response to acetaminophen is not satisfactory or the clinical presentation is inflammatory, consider nonsteroidal
anti-inflammatory drugs (NSAIDs). (See Medication.) If all other modalities are ineffective and osteotomy is not viable, or if a
patient cannot perform his or her daily activities despite maximal therapy, arthroplasty is indicated.

The high prevalence of osteoarthritis entails significant costs to society. Direct costs include clinician visits, medications,
therapeutic modalities, and surgical intervention. Indirect costs include such items as time lost from work.

Costs associated with osteoarthritis can be particularly significant for elderly persons, who face potential loss of independence
and who may need help with daily living activities. As the populations of developed nations age over the coming decades, the
need for better understanding of osteoarthritis and for improved therapeutic alternatives will continue to grow. (See
Epidemiology.)

Anatomy
Joints can be classified in either functional or structural terms. A functional classification, based on movement, would
categorize joints as follows:

Synarthroses (immovable)
Amphiarthroses (slightly moveable)
Diarthroses (freely moveable)

A structural classification would categorize joints as follows:

Synovial
Fibrous
 Cartilaginous

Normal synovial joints allow a significant amount of motion along their extremely smooth articular surface. These joints are
composed of the following:

Articular cartilage
Subchondral bone
Synovial membrane
Synovial fluid
Joint capsule

The normal articular surface of synovial joints consists of articular cartilage (composed of chondrocytes) surrounded by an
extracellular matrix that includes various macromolecules, most importantly proteoglycans and collagen. The cartilage
facilitates joint function and protects the underlying subchondral bone by distributing large loads, maintaining low contact
stresses, and reducing friction at the joint.

Synovial fluid is formed through a serum ultrafiltration process by cells that form the synovial membrane (synoviocytes).
Synovial cells also manufacture hyaluronic acid (HA, also known as hyaluronate), a glycosaminoglycan that is the major
noncellular component of synovial fluid. Synovial fluid supplies nutrients to the avascular articular cartilage; it also provides the
viscosity needed to absorb shock from slow movements, as well as the elasticity required to absorb shock from rapid
movements.

Pathophysiology
Primary and secondary osteoarthritis are not separable on a pathologic basis, though bilateral symmetry is often seen in cases
of primary osteoarthritis, particularly when the hands are affected.[3, 23] Traditionally, osteoarthritis was thought to affect
primarily the articular cartilage of synovial joints; however, pathophysiologic changes are also known to occur in the synovial
fluid, as well as in the underlying (subchondral) bone, the overlying joint capsule, and other joint tissues (see Workup).[24, 25, 26,
27]

Although osteoarthritis has been classified as a noninflammatory arthritis, increasing evidence has shown that inflammation
occurs as cytokines and metalloproteinases are released into the joint. These agents are involved in the excessive matrix
degradation that characterizes cartilage degeneration in osteoarthritis.[28] Therefore, it is no longer appropriate to use the term
degenerative joint disease when referring to osteoarthritis.

Studies of interleukin-17 (IL-17), a proinflammatory cytokine, have found increased IL-17 levels in the synovium of osteoarthritis
joints, as is seen in inflammatory arthritis (ie, rheumatoid arthritis).[29]  Other inflammatory molecules that have been
associated with osteoarthritis include 15‐hydroxyeicosatetraenoic acid, prostaglandin E2, IL‐1β, IL‐1 receptor antagonist, and
uric acid.[30]  

In early osteoarthritis, swelling of the cartilage usually occurs, because of the increased synthesis of proteoglycans; this reflects
an effort by the chondrocytes to repair cartilage damage. This stage may last for years or decades and is characterized by
hypertrophic repair of the articular cartilage.

As osteoarthritis progresses, however, the level of proteoglycans eventually drops very low, causing the cartilage to soften and
lose elasticity and thereby further compromising joint surface integrity. Microscopically, flaking and fibrillations (vertical clefts)
develop along the normally smooth articular cartilage on the surface of an osteoarthritic joint. Over time, the loss of cartilage
results in loss of joint space.

In major weight-bearing joints of persons with osteoarthritis, a greater loss of joint space occurs at those areas experiencing the
highest loads. This effect contrasts with that of inflammatory arthritides, in which uniform joint-space narrowing is the rule.

In the osteoarthritic knee, for example, the greatest loss of joint space is commonly seen in the medial femorotibial
compartment, though the lateral femorotibial compartment and patellofemoral compartment may also be affected. Collapse of
the medial or lateral compartments may result in varus or valgus deformities, respectively.

Krasnokutsky et al reported that the serum uric acid level can predict future joint space narrowing. In their study of 88 patients
with medial knee osteoarthritis, over the course of 24 months, mean joint space narrowing of 0.31 mm occurred in patients with
a serum uric acid level of less than 6.8 mg/dL (the solubility point for serum urate), compared with 0.90 mm in those with a
serum uric acid level of 6.8 mg/dL or higher (P <  0.01). These authors suggest that serum uric acid levels may serve as a
biomarker for progression of osteoarthritis.[30]
Erosion of the damaged cartilage in an osteoarthritic joint progresses until the underlying bone is exposed. Bone denuded of its
protective cartilage continues to articulate with the opposing surface. Eventually, the increasing stresses exceed the
biomechanical yield strength of the bone. The subchondral bone responds with vascular invasion and increased cellularity,
becoming thickened and dense (a process known as eburnation) at areas of pressure.[31]

The traumatized subchondral bone may also undergo cystic degeneration, which is attributable either to osseous necrosis
secondary to chronic impaction or to the intrusion of synovial fluid. Osteoarthritic cysts are also referred to as subchondral
cysts, pseudocysts, or geodes (the preferred European term) and may range from 2 to 20 mm in diameter. Osteoarthritic cysts in
the acetabulum (see the image below) are termed Egger cysts.

Anteroposterior (AP) radiograph of the hip reveals severe superior migration of the femoral head (which reflects loss of
articular cartilage), subchondral sclerosis, prominent osteophytes, and a large Egger cyst in the superior acetabulum. Mild
flattening of the superior aspect of the femoral head is present.

At areas along the articular margin, vascularization of subchondral marrow, osseous metaplasia of synovial connective tissue,
and ossifying cartilaginous protrusions lead to irregular outgrowth of new bone (osteophytes). Fragmentation of these
osteophytes or of the articular cartilage itself results in the presence of intra-articular loose bodies (joint mice).

Along with joint damage, osteoarthritis may also lead to pathophysiologic changes in associated ligaments and the
neuromuscular apparatus. For example, lateral collateral ligament complex abnormalities are common in knee osteoarthritis.

Pain mechanisms in osteoarthritis

Pain, the main presenting symptom of osteoarthritis, is presumed to arise from a combination of mechanisms, including the
following:

Osteophytic periosteal elevation

Vascular congestion of subchondral bone, leading to increased intraosseous pressure

Synovitis with activation of synovial membrane nociceptors

Fatigue in muscles that cross the joint

Overall joint contracture

Joint effusion and stretching of the joint capsule

Torn menisci

Inflammation of periarticular bursae

Periarticular muscle spasm

Psychological factors

Crepitus (a rough or crunchy sensation)

 Central pain sensitization

When the spine is involved in osteoarthritis, especially the lumbar spine, the associated changes are very commonly seen from
L3 through L5. Symptoms include pain, stiffness, and occasional radicular pain from spinal stenosis. Foraminal narrowing is
caused by facet arthritic changes that result in compression of the nerve roots. Acquired spondylolisthesis is a common
complication of arthritis of the lumbar spine.

Etiology
The daily stresses applied to the joints, especially the weight-bearing joints (eg, ankle, knee, and hip), play an important role in
the development of osteoarthritis. Most investigators believe that degenerative alterations in osteoarthritis primarily begin in the
articular cartilage, as a result of either excessive loading of a healthy joint or relatively normal loading of a previously disturbed
joint. External forces accelerate the catabolic effects of the chondrocytes and further disrupt the cartilaginous matrix.[32, 33, 34,
35]

Risk factors for osteoarthritis include the following[36, 37, 38, 39] :

Age

Obesity[40, 41, 42]

Trauma

Genetics (significant family history)

Reduced levels of sex hormones

Muscle weakness[43]

Repetitive use (ie, jobs requiring heavy labor and bending)[44]

Infection

Crystal deposition

Acromegaly

Previous inflammatory arthritis (eg, burnt-out rheumatoid arthritis)

Heritable metabolic causes (eg, alkaptonuria, hemochromatosis, Wilson disease)

Hemoglobinopathies (eg, sickle cell disease and thalassemia)

Neuropathic disorders leading to a Charcot joint (eg, syringomyelia, tabes dorsalis, and diabetes)

Underlying morphologic risk factors (eg, congenital hip dislocation and slipped femoral capital epiphysis)

Disorders of bone (eg, Paget disease and avascular necrosis)

Previous surgical procedures (eg, meniscectomy)

Diabetes mellitus[45]

Advancing age

With advancing age come reductions in cartilage volume, proteoglycan content, cartilage vascularization, and cartilage
perfusion. These changes may result in certain characteristic radiologic features, including a narrowed joint space and marginal
osteophytes. However, biochemical and pathophysiologic findings support the notion that age alone is an insufficient cause of
osteoarthritis.

Senescent cells (SnCs) accumulate in many tissues with age and contribute to age-related pathologies. A study in mice by Jeon
et al found that SnCs accumulated in the articular cartilage and synovium after anterior cruciate ligament transection, and
selective elimination of SnCs attenuated the development of post-traumatic osteoarthritis, reduced pain, and increased cartilage
development. In addition, selective removal of SnCs from in vitro cultures of chondrocytes isolated from patients with
osteoarthritis undergoing total knee replacement resulted in decreased expression of senescent and inflammatory markers and
increased expression of cartilage tissue extracellular matrix proteins.[46]

Obesity

Obesity increases the mechanical stress in a weight-bearing joint. It has been strongly linked to osteoarthritis of the knees and,
to a lesser extent, of the hips. A study that evaluated the associations between body mass index (BMI) over 14 years and knee
pain at year 15 in 594 women found that a higher BMI at year 1 and a significant increase in BMI over 15 years were predictors
of bilateral knee pain at year 15.[42] The association between BMI increase and knee pain was independent of radiographic
changes.

In addition to its mechanical effects, obesity may be an inflammatory risk factor for osteoarthritis. Obesity is associated with
increased levels (both systemic and intra-articular) of adipokines (cytokines derived from adipose tissue), which may promote
chronic, low-grade inflammation in joints.[47]

Other causes

Trauma or surgery (including surgical repair of traumatic injury) involving the articular cartilage, ligaments, or menisci can lead
to abnormal biomechanics in the joints and accelerate osteoarthritis. In individuals who have sustained significant joint injuries,
the risk of post-traumatic osteoarthritis ranges from about 20% to more than 50%.[48]

Insults to the joints may occur even in the absence of obvious trauma. Microtrauma may also cause damage, especially in
individuals whose occupation or lifestyle involves frequent squatting, stair-climbing, or kneeling.

Muscle dysfunction compromises the body’s neuromuscular protective mechanisms, leading to increased joint motion and
ultimately resulting in osteoarthritis. This effect underscores the need for continued muscle toning exercises as a means of
preventing muscle dysfunction.

Valgus malalignment at the knee has been shown to increase the incidence and risk of radiographic progression of knee
osteoarthritis involving the lateral compartment.[49]

Genetics

A hereditary component, particularly in osteoarthritis presentations involving multiple joints, has long been recognized.[50, 51,
52] Several genes have been directly associated with osteoarthritis,[53] and many more have been determined to be associated
with contributing factors, such as excessive inflammation and obesity.

Osteoarthritis susceptibility genes (eg, ADAM12, CLIP, COL11A2, IL10, MMP3) have also been found to have differential
methylation. Jefferies et al reports that hypomethylation of FURIN, which encodes a proprotein convertase, processes several
ADAMTS molecules involved in osteoarthritic collagen degradation. Differential methylation among osteoarthritis susceptibility
genes has been proposed as an alternative method for disruption of normal gene activity.

Additionally, Jefferies et al found evidence for hypermethylation and reduced expression of the type XI collagen gene COL11A2.
Mutations involving COL11A2 have been associated with severe and early-onset osteoarthritis. Analysis by this goup has
identified pathways enriched with "differentially methylated genes" that are effectors and upstream regulators seen in
osteoarthritis linked with TGFB1 and ERG.[54]

Genes in the BMP (bone morphogenetic protein) and WNT (wingless-type) signaling cascades have been implicated in
osteoarthritis. Two genes in particular, GDF5 (growth and differentiation factor 5) and FRZB (frizzled related protein), have been
identified in the articular cartilage in animal studies and share a strong correlation with osteoarthritis.[55, 56, 57, 58]

Genome-wide association studies (GWAS) have identified an association between osteoarthritis of large joints and the MCF2L
gene. This gene is key in neurotrophin-mediated regulation of peripheral nervous system cell motility.[59]

Genetic factors are also important in certain heritable developmental defects and skeletal anomalies that can cause congenital
misalignment of joints. These may result in damage to cartilage and the structure of the joint.

Currently, clinical genetic testing is not offered to patients who have osteoarthritis unless they also have other anomalies that
could be associated with a genetic condition. In the future, testing may allow individualization of therapeutics.
Epidemiology
United States and international statistics

Osteoarthritis affects more than 20 million individuals in the United States, though statistical figures are influenced by how the
condition is defined—that is, by self-report, by radiographic or symptomatic criteria, or by a combination of these.[60] On the
basis of the radiographic criteria for osteoarthritis, more 50% of adults older than 65 years are affected by the disease.

Internationally, osteoarthritis is the most common articular disease. Estimates of its frequency vary across different
populations.

Age-related demographics

Primary osteoarthritis is a common disorder of the elderly, and patients are often asymptomatic. Approximately 80-90% of
individuals older than 65 years have evidence of radiographic primary osteoarthritis.[61]

Symptoms typically do not become noticeable until after the age of 50 years. The prevalence of the disease increases
dramatically among persons older than 50 years, likely because of age-related alterations in collagen and proteoglycans that
decrease the tensile strength of the joint cartilage and because of a diminished nutrient supply to the cartilage.[61]

Sex-related demographics

In individuals older than 55 years, the prevalence of osteoarthritis is higher among women than among men.[61] Women are
especially susceptible to osteoarthritis in the DIP joints of the fingers. Women also have osteoarthritis of the knee joints more
frequently than men do, with a female-to-male incidence ratio of 1.7:1. Women are also more prone to erosive osteoarthritis,
with a female-to-male ratio of about 12:1.

Race-related demographics

Interethnic differences in the prevalence of osteoarthritis have been noted.[62] The disorder is more prevalent in Native
Americans than in the general population. Disease of the hip is seen less frequently in Chinese patients from Hong Kong than in
age-matched white populations. Symptomatic knee osteoarthritis is extremely common in China.[63]

In persons older than 65 years, osteoarthritis is more common in whites than in blacks. Knee osteoarthritis appears to be more
common in black women than in other groups. Jordan et al found that in comparison with whites, African American men and
women had a slightly higher prevalence of radiographic and symptomatic knee osteoarthritis but a significantly higher
prevalence of severe radiographic knee osteoarthritis.[64]

Prognosis
The prognosis in patients with osteoarthritis depends on the joints involved and on the severity of the condition. No proven
disease-modifying or structure-modifying drugs for osteoarthritis are currently known; consequently, pharmacologic treatment is
directed at symptom relief.

A systematic review found the following clinical features to be associated with more rapid progression of knee osteoarthritis[65]
:

Older age

Higher BMI

Varus deformity

Multiple involved joints

Patients with osteoarthritis who have undergone joint replacement have a good prognosis, with success rates for hip and knee
arthroplasty generally exceeding 90%. However, a joint prosthesis may have to be revised 10-15 years after its placement,
depending on the patient’s activity level. Younger and more active patients are more likely to require revisions, whereas the
majority of older patients will not. (See Treatment.)
Patient Education
Educate patients on the natural history of and management options for osteoarthritis, emphasizing the benefits of exercise and
weight loss. Explain the differences between osteoarthritis and more rapidly progressive arthritides, such as rheumatoid
arthritis.

Several Arthritis Foundation studies have demonstrated that education in osteoarthritis benefits the patient. Through education,
patients can learn and implement strategies for reducing pain and improving joint function. Emphasize the need for physician
follow-up visits.

For patient education information, see the Arthritis Center, as well as Osteoarthritis.

Presentation

History
The progression of osteoarthritis is characteristically slow, occurring over several years or decades. Over this period, the patient
can become less and less active and thus more susceptible to morbidities related to decreasing physical activity (including
potential weight gain).

Early in the disease process, the joints may appear normal. However, the patient’s gait may be antalgic if weight-bearing joints
are involved.

Pain is usually the initial source of morbidity in osteoarthritis, with the disease’s primary symptom being deep, achy joint pain
exacerbated by extensive use. Also, reduced range of motion and crepitus are frequently present. Stiffness during rest (gelling)
may develop, with morning joint stiffness usually lasting for less than 30 minutes.

Initially, pain can be relieved by rest and may respond to simple analgesics. However, joints may become unstable as the
osteoarthritis progresses; therefore, the pain may become more prominent (even during rest) and may not respond to
medications.

Physical Examination
Physical examination findings in patients with osteoarthritis are mostly limited to the affected joints.[66, 67, 68] Reduced range
of motion and crepitus are frequently present.

Malalignment with a bony enlargement may occur. Most cases of osteoarthritis do not involve erythema or warmth over the
affected joint(s); however, a bland effusion may be present. Limitation of joint motion or muscle atrophy around a more severely
affected joint may occur.

Osteoarthritis of the hand most often affects the distal interphalangeal (DIP) joints but also typically involves the proximal
interphalangeal (PIP) joints and the joints at the base of the thumb. Heberden nodes, which represent palpable osteophytes in
the DIP joints, are more characteristic in women than in men. Inflammatory changes are typically absent or at least not
pronounced.

Progression of Osteoarthritis
The etiopathogenesis of osteoarthritis has been divided into three stages, as follows:

Stage 1 – Proteolytic breakdown of the cartilage matrix occurs

Stage 2 – Fibrillation and erosion of the cartilage surface develop, with subsequent release of proteoglycan and collagen
fragments into the synovial fluid

Stage 3 – Breakdown products of cartilage induce a chronic inflammatory response in the synovium, which in turn
contributes to further cartilage breakdown

Several systems have been advocated for use in the grading of focal cartilage change; however, a simple description of the
extent of disease (ie, surface, partial-thickness, or full-thickness irregularity with or without underlying subchondral bone
change) is generally sufficient and prevents the confusion that may occur with numeric grading systems. Such systems are in
any case intended more for research purposes than for clinical use.

Certain diseases are often categorized as subsets of primary osteoarthritis. These include primary generalized osteoarthritis
(PGOA), erosive osteoarthritis, and chondromalacia patellae.

Hand osteoarthritis has been classified as follows:

Erosive

Thumb base

Interphalangeal (with or without nodes)

Widespread hand

Marshall et al report that thumb base osteoarthritis tends to be most prevalent symptomatic form of hand osteoarthritis,
followed by interphalangeal joint osteoarthritis. Erosive and generalized hand osteoarthritis were found in older populations and
predominantly in women. Over time, erosive osteoarthritis tends to have the poorest characteristics and leads to the most
disability.[69]

For more information, see Progression of Osteoarthritis.

DDx

Diagnostic Considerations
The initial diagnostic goal is to differentiate osteoarthritis from other arthritides, such as rheumatoid arthritis. The history and
physical examination findings are usually sufficient to diagnose osteoarthritis. Radiographic findings confirm the initial
impression (see Workup), and laboratory values are typically within the reference range.

Rheumatoid arthritis
Rheumatoid arthritis predominantly affects the wrists, as well as the metacarpophalangeal (MCP) and proximal interphalangeal
(PIP) joints. It rarely, if ever, involves the distal interphalangeal (DIP) joints or the lumbosacral spine.

Rheumatoid arthritis is associated with prominent, prolonged (>1 hour) morning stiffness and overtly swollen, warm joints.
Radiographic findings include bone erosion (eg, periarticular osteopenia or marginal erosions of bone) rather than formation.
Laboratory findings that further differentiate rheumatoid arthritis from osteoarthritis include the following:

Systemic inflammation (elevated erythrocyte sedimentation rate [ESR] or C-reactive protein [CRP] level)

Positive serologies (rheumatoid factor [RF] or anti–cyclic citrullinated peptide [anti-CCP] antibodies)

Inflammatory joint fluid with a predominance of polymorphonuclear leukocytes (PMNs)

Elevated white blood cell (WBC) count

Other arthritides
Back pain may result from spondyloarthropathy or from osteoarthritis with sacroiliac and lumbosacral spine involvement.
Clinical history and characteristic radiographic findings can be used to differentiate these disorders.

Secondary osteoarthritis must be considered in individuals with any of the following:

Chondrocalcinosis

History of joint trauma

Metabolic bone disorders

Hypermobility syndromes

Neuropathic diseases

The following disorders should also be considered in the differential diagnosis:

Crystalline arthropathies (ie, gout and pseudogout)

Inflammatory arthritis (eg, rheumatoid arthritis)

Seronegative spondyloarthropathies (eg, psoriatic arthritis and reactive arthritis)

Septic arthritis or postinfectious arthropathy

Fibromyalgia

Tendonitis

In patients with knee pain, other disorders to consider in the differential diagnosis are patellofemoral syndrome and prepatellar
bursitis.

Differential Diagnoses
Avascular Necrosis

Fibromyalgia

Gout and Pseudogout

Imaging in Ankylosing Spondylitis

Imaging in Neuropathic Arthropathy (Charcot Joint)

Lyme Disease

Patellofemoral Arthritis

Psoriatic Arthritis

Rheumatoid Arthritis

Workup
 

Workup

Approach Considerations
Osteoarthritis is typically diagnosed on the basis of clinical and radiographic evidence.[3, 4, 5, 6, 7] No specific laboratory
abnormalities are associated with osteoarthritis.

Researchers have investigated the use of monoclonal antibodies, synovial fluid markers, and urinary pyridinium cross-links (ie,
breakdown products of cartilage) as osteoarthritic indicators.[70] No single biomarker has proved reliable for diagnosis and
monitoring, but combinations of cartilage-derived and bone-derived biomarkers have been used to identify osteoarthritis
subtypes, with possible impact on treatment.[71]

Levels of acute-phase reactants are typically within the reference range in patients with osteoarthritis. The erythrocyte
sedimentation rate (ESR) is not usually elevated, though it may be slightly so in cases of erosive inflammatory arthritis. The
synovial fluid analysis usually shows a white blood cell (WBC) count below 2000/µL, with a mononuclear predominance.

Plain Radiography
Plain radiography is the imaging method of choice because it is more cost-effective than other modalities and because
radiographs can be obtained more readily and quickly.[5, 8] One important characteristic of primary osteoarthritis is that the
abnormalities found in the load-bearing (ie, highly stressed) areas of the affected joint differ from those found in the non–load-
bearing areas. In the load-bearing areas, radiographs can depict joint-space loss, as well as subchondral bony sclerosis and cyst
formation (see the image below).

This radiograph demonstrates osteoarthritis of the right hip, including the finding of sclerosis at the superior aspect of the
acetabulum. Frequently, osteoarthritis at the hip is a bilateral finding, but it may occur unilaterally in an individual who has a
previous history of hip trauma that was confined to that one side.

The elbow is not commonly affected in osteoarthritis. However, elbow arthritis (see the images below) can occur as a result of
trauma.
Osteoarthritis of the elbow is not commonly seen; however, it can occur with a history of previous trauma.

Osteoarthritis of the elbow is not commonly seen; however, it can occur with a history of previous trauma.

Osteoarthritis of the elbow is not commonly seen; however, it can occur with a history of previous trauma.

MRI, CT, and Ultrasonography

Magnetic resonance imaging (MRI) can depict many of the same characteristics of osteoarthritis that plain radiography can, but
it is not necessary in most patients with osteoarthritis, unless additional pathology amenable to surgical repair is suspected.
Pathology that can be seen on MRI includes joint narrowing, subchondral osseous changes, and osteophytes. Unlike
radiography, MRI can directly visualize articular cartilage and other joint tissues (eg, meniscus, tendon, muscle, or effusion).

Computed tomography (CT) is rarely used in the diagnosis of primary osteoarthritis. However, it may be used in the diagnosis of
malalignment of the patellofemoral joint or of the foot and ankle joints.

Currently, ultrasonography has no role in the routine clinical assessment of the patient with osteoarthritis. However, it is being
investigated as a tool for monitoring cartilage degeneration, and it can be used for guided injections of joints not easily
accessed without imaging.
For more information, see Imaging in Osteoarthritis.

Bone Scanning
Bone scans may be helpful in the early diagnosis of osteoarthritis of the hand.[9] Bone scans in osteoarthritis typically yield a
symmetrically patterned, very mildly increased uptake. In contrast, bone scans are often negative in the early stages of multiple
myeloma, a cause of bone pain in older adults that can be confused with osteoarthritis. Bone scans also can help to
differentiate osteoarthritis from osteomyelitis and bone metastases.

Arthrocentesis
A diagnostic joint aspiration for synovial fluid analysis can help exclude inflammatory arthritis, infection, or crystal arthropathy.
The presence of noninflammatory joint fluid helps distinguish osteoarthritis from other causes of joint pain. Other synovial fluid
findings that aid in the differentiation of osteoarthritis from other conditions are negative Gram stains and cultures, as well as
the absence of crystals when fluid is viewed under a polarized microscope.

For more information, see the following:

Knee Arthrocentesis

Metacarpophalangeal Arthrocentesis

Shoulder Arthrocentesis

Treatment

Approach Considerations
The goals of osteoarthritis treatment include alleviation of pain and improvement of functional status. Optimally, patients should
receive a combination of nonpharmacologic and pharmacologic treatment.[72]

Nonpharmacologic interventions, which are the cornerstones of osteoarthritis therapy, include the following:

Patient education
Heat and cold
Weight loss [10]
Exercise
Physical therapy
Occupational therapy
Unloading in certain joints (eg, knee, hip)

A physiatrist may help in formulating a nonpharmacologic management plan for the patient with osteoarthritis, and a nutritionist
may help the patient to lose weight. A referral to an orthopedic surgeon may be necessary if the osteoarthritis fails to respond to
a medical management plan. Surgical procedures for osteoarthritis include arthroscopy, osteotomy, and (particularly with knee
or hip osteoarthritis) arthroplasty.

Several organizations have issued guidelines on the treatment of osteoarthrits (see Guidelines), with recommendations keyed to
the affected joints (ie, hand, knee, hip). An assessment of several treatments for osteoarthritis of the knee by the Agency for
Healthcare Research and Quality (AHRQ) determined the following[73] :
 Home-based exercise programs and tai chi show short- to medium-term benefits for symptoms (primarily pain, function,
and quality of life) but data on long-term benefits are lacking
Strength and resistance training, pulsed electromagnetic field therapy, and transcutaneous electrical nerve stimulation
show mostly short-term benefits, whereas agility training shows both short- and long-term benefits.
Weight loss and general exercise programs show medium- and long-term benefits.
Intra-articular platelet-rich plasma, balneotherapy, and whole-body vibration show medium-term benefits.
Glucosamine-chondroitin and glucosamine or chondroitin sulfate alone show medium-term benefits with no long-term
benefits for pain or function.

Mesenchymal stem cell therapy continues to be a promising investigational approach to knee osteoarthritis.[74, 75]  However,
the improvement reported with stem cell therapy has been modest, a placebo effect remains possible, and the quality of the
supporting evidence has been questioned.[76, 77]  In addition, the variability in mesenchymal stem cell injection, including
timing, frequency, and culturing mode,  warrant further research, as does the possible long-term risk. 

Pharmacologic Treatment
Analgesics and anti-inflammatory drugs

Begin treatment with acetaminophen for mild or moderate osteoarthritic pain without apparent inflammation. If the clinical
response to acetaminophen is not satisfactory or if the clinical presentation of osteoarthritis is inflammatory, consider using a
nonsteroidal anti-inflammatory drug (NSAID). Use the lowest effective dose or intermittent dosing if symptoms are intermittent,
then try full doses if the patient’s response is insufficient.

Topical NSAID preparations, particularly diclofenac, are available. These preparations can be particularly useful in patients with
symptomatic disease that is limited to a few sites or in patients who are at increased risk for adverse events with systemic
NSAIDs.

In patients with highly resistant pain, consider the analgesic tramadol. However, in an observational study of more than 88,000
patients, an initial prescription of tramadol was associated with a significantly higher rate of mortality over 1 year of follow-up
compared with commonly prescribed NSAIDs in patients aged 50 years and older.[78]  The data from this study suggest an
unfavorable safety profile of tramadol and require replication. Differences between the study groups (eg, cancer) that were not
adjusted away using propensity score matching may account for part or even all of the difference in mortality rates.[79]

Options in patients at an elevated risk for GI toxicity from NSAIDs include the addition of a proton-pump inhibitor or misoprostol
to the treatment regimen. Clinicians may also consider prescribing the selective cyclooxygenase (COX)-2 inhibitor celecoxib
instead of a nonselective NSAID.

In June 2018, the US Food and Drug Administration (FDA) approved the combination of the calcium channel blocker amlodipine
with celecoxib (Consensi), for patients for whom treatment with amlodipine for hypertension and celecoxib for osteoarthritis are
appropriate. Lowering blood pressure reduces the risk of fatal and nonfatal cardiovascular events, primarily strokes and
myocardial infarctions, which is elevated in patients taking celecoxib.[80]

Hydroxychloroquine, which is approved for use in rheumatoid arthritis, has been used off-label in patients with hand
osteoarthritis, on the supposition that it might help by relieving synovitis. However, a randomized study in 210 patients found
that hydroxychloroquine does not improve symptoms of hand osteoarthritis.[81]

Study patients had experienced insufficient response to, or adverse effects from, analgesics such as acetaminophen, NSAIDs, or
opioids, and were randomized to receive hydroxychloroquine (usually 300 mg/day) or placebo for 12 months, in addition to their
usual analgesic medications. At 6 months, there were no significant differences between hydroxychloroquine and placebo
recipients in hand pain—the primary outcome—or in grip strength and structural damage.

Agency for Healthcare Research and Quality findings

A 2011 comparison of analgesics for osteoarthritis carried out by the Agency for Healthcare Research and Quality (AHRQ) found
that “no currently available analgesic reviewed in this report offers a clear overall advantage compared with the others.”[82]  The
choice of analgesic for an individual patient should take into account the trade-off between benefits and adverse effects, which
differs across analgesics. Patient age, comorbid conditions, and concomitant medication are key considerations.

The AHRQ comparison found that acetaminophen was modestly inferior to NSAIDs in reducing osteoarthritic pain but was
associated with a lower risk of GI adverse effects.[82] On the other hand, acetaminophen poses a higher risk of liver injury.

AHRQ findings on adverse effects included the following:

 Selective NSAIDs as a class were associated with a lower risk of ulcer complications than were the nonselective NSAIDs
naproxen, ibuprofen, and diclofenac

The partially selective NSAIDs meloxicam and etodolac were associated with a lower risk of ulcer-related complications
and symptomatic ulcers than were various nonselective NSAIDs

The risk of serious GI adverse effects was found to be higher with naproxen than with ibuprofen

Celecoxib and the nonselective NSAIDs ibuprofen and diclofenac were associated with an increased risk of
cardiovascular adverse effects when compared with placebo

The nonselective NSAIDs ibuprofen and diclofenac, but not naproxen, were associated with an increased risk of heart
attack when compared with placebo

The AHRQ noted that topical diclofenac was found to have efficacy similar to that of oral NSAIDs in patients with localized
osteoarthritis. No head-to-head trials compared topical salicylates or capsaicin with oral NSAIDs for osteoarthritis.[82]

All NSAIDs had deleterious effects on blood pressure, edema, and kidney function. However, the AHRQ found no consistent
clinically relevant differences between celecoxib, partially selective NSAIDs, and nonselective NSAIDs with regard to the risk of
hypertension, heart failure, or impaired kidney function.[82]

Duloxetine
The selective serotonin-norepinephrine reuptake inhibitor duloxetine has been found to be effective in treating osteoarthritis
pain.[83] For example, in patients with knee osteoarthritis who had persistent moderate pain despite optimized NSAID therapy, a
randomized, double-blind trial found significant additional pain reduction and functional improvement with duloxetine as
compared with placebo.[84]

However, duloxetine was also associated with significantly more nausea, dry mouth, constipation, fatigue, and decreased
appetite than placebo was.[84] To date, trials of duloxetine in osteoarthritis have been short in duration (10-13 weeks), and
studies comparing duloxetine directly with other therapies have not been performed.

Intra-articular injections

Intra-articular pharmacologic therapy includes injection of a corticosteroid or sodium hyaluronate (ie, hyaluronic acid [HA] or
hyaluronan) or biologic agent (ie, platelet-rich plasma [PRP]), which may provide pain relief and have an anti-inflammatory effect
on the affected joint.[85, 86] Ultrasound guidance can facilitate arthrocentesis and injection and is increasingly being adopted by
physicians such as rheumatologists and physiatrists for this purpose.

Corticosteroid

After the introduction of the needle into the joint and before steroid administration, aspiration of as much synovial fluid as
possible should be attempted. Aspiration often provides symptomatic relief for the patient and allows laboratory evaluation of
the fluid, if necessary. Infected joint fluid and bacteremia are contraindications to steroid injection.

In patients with osteoarthritic knee pain, steroid injections generally result in clinically and statistically significant pain reduction
as soon as 1 week after injection. The effect may last, on average, anywhere from 4 to 6 weeks per injection, but the benefit is
unlikely to continue beyond that time frame.[87]  

However, in a randomized trial by McAlindon et al comprising 140 patients with symptomatic knee osteoarthritis with synovitis,
intra-articular injections of steroid (40 mg triamcinolone, every 12 weeks for 2 years) resulted in significantly greater cartilage
volume loss and no significant difference in knee pain, compared with placebo injections of saline. The authors concluded that
their findings do not support the use of intra-articular steroid injections for symptomatic knee osteoarthritis.[88, 89]

In October 2017, the FDA approved triamcinolone acetonide extended-release injectable suspension (Zilretta) for intra-articular
treatment of osteoarthritic knee pain. Approval was based on data from a randomized, double-blind international phase III trial in
which 484 patients were treated and followed for up to 24 weeks. Patients receiving Zilretta reported a statistically significant
reduction in the weekly mean of the average daily pain intensity scores (ADP) from baseline to week 12.[90]

For hip osteoarthritis, a randomized, placebo-controlled study confirmed the effectiveness of corticosteroid injection, with
benefits often lasting as long as 3 months.[91]

Some controversial evidence exists regarding frequent steroid injections and subsequent damage to cartilage
(chondrodegeneration). Accordingly, it is usually recommended that no more than three injections per year be delivered to any
individual osteoarthritic joint. Systemic glucocorticoids have no role in the management of osteoarthritis.

For more information, see Corticosteroid Injections of Joints and Soft Tissues.
Sodium hyaluronate

Intra-articular injection of sodium hyaluronate, also referred to as viscosupplementation, has been shown to be safe and
possibly effective for symptomatic relief of knee osteoarthritis.[92, 93] In the United States, intra-articular HAs are classified as
medical devices rather than as drugs.[94]

Intra-articular HAs approved by the FDA for the treatment of osteoarthritic knee pain include the naturally extracted, non–cross-
linked sodium hyaluronate products Hyalgan,[95] Supartz, Orthovisc, and Euflexxa, as well as the cross-linked sodium
hyaluronate product known as hylan G-F 20 (Synvisc).

Euflexxa is derived from a fermentation process (Streptococcus), whereas the source material for the other products listed is
chicken combs. At present, no distinct advantage or disadvantage has been associated with any particular source of HA.

Some differences between the viscosupplements do exist in the FDA-approved prescribing information. For example, whereas
Hyalgan and Synvisc have been established as safe for repeat treatment, the safety and efficacy of other products for repeat
treatment have not been established.

The exact mechanisms of action through which HAs provide symptomatic relief are unknown. Possible mechanisms include
direct binding to receptors (CD44 in particular) in the synovium and cartilage that can lead to several biologic activation
pathways.[96, 97]

The HA class in general has demonstrated a very favorable safety profile for chronic pain management in knee osteoarthritis,
with the most common adverse event being injection-site pain. Although any intra-articular injection (whether of HAs or of
steroids) may elicit an inflammatory response and possible effusion, only the cross-linked hylan G-F 20 product has been
associated with a clinically distinct acute inflammatory side effect (ie, severe acute inflammatory reaction [SAIR] or HA-
associated intra-articular pseudosepsis).

Platelet-rich plasma

PRP is defined as a volume of plasma with a platelet concentration higher than the average in peripheral blood (150,000–
350,000 platelets/μl).[98]  A meta-analysis of 10 randomized controlled trials (RCTs) with a total of 1069 patients found
that intra-articular PRP injection may have more benefit in pain relief and functional improvement than hyaluronic acid or saline
in patients with symptomatic knee osteoarthritis at 1 year postinjection.[99]  However, concerns have been raised regarding its
clinical efficacy, mainly due to the heterogeneity of preparation methods and resulting products, the scarceness of high-quality
RCTs, and the contradictory results that have been found so far.[100]  

The FDA has cleared PRP preparation systems as a device ‘substantially equivalent’ to another device previously cleared.
However, the clearance applies only to the device and its intended use in an operative setting and makes no claim about its
effectiveness for a particular indication. Similarly, in the European Union, only the preparation procedure, and not the product
itself, is regulated, and the regulation does not include any requirements about the composition or effectiveness of PRP.[98]

Prolotherapy

In prolotherapy, small volumes of an irritant solution are injected at ligament and tendon insertions and in adjacent joint spaces
over several treatment sessions. In a randomized, controlled trial of 90 adults with painful knee osteoarthritis who were
randomized to either dextrose prolotherapy, saline injections, or at-home exercise, the patients on prolotherapy experienced
significantly greater improvement in pain, function, and stiffness over the other 2 groups. Injections were administered at 1, 5,
and 9 weeks, with additional injections provided as needed at weeks 13 and 17.[101]

Additional pharmacologic agents

Muscle relaxants may benefit patients with evidence of muscle spasm. Judicious use of narcotics (eg, oxycodone and
acetaminophen with codeine) is reserved for patients with severe osteoarthritis.

Glucosamine and chondroitin sulfate have been used in Europe for many years and continue to be popular with patients
worldwide. In the United States, however, the glucosamine/chondroitin arthritis intervention trial (GAIT) reported, at best, limited
benefit from glucosamine (500 mg 3 times daily), chondroitin sulfate (400 mg 3 times daily), or the combination of the 2 in
patients with knee osteoarthritis.[102, 103]

In GAIT patients overall, glucosamine and chondroitin sulfate alone or in combination did not reduce pain effectively at 24
weeks, but in patients with moderate-to-severe pain at baseline, the rate of response was significantly higher with combined
therapy than with placebo (79.2% vs. 54.3%).[103] At 2 years, no treatment achieved a clinically important difference in loss of
joint-space width, though treatment effects on Kellgren-Lawrence grade 2 knees showed a trend toward improvement relative to
the placebo group.[102]

The AHRQ comparison found no clear difference between glucosamine or chondroitin and oral NSAIDs for relieving pain or
improving function.[82] However, the AHRQ observed that most trials showing therapeutic benefits from glucosamine used
pharmaceutical-grade glucosamine that is not available in the United States, noting that the trial findings may therefore be
inapplicable to currently available over-the-counter preparations.

Another agent, S-adenosylmethionine (SAM-e), is a European supplement receiving significant attention in the United States. A
systematic review of SAM-e found that the evidence was inconclusive, with a number of small trials of questionable quality; the
authors concluded that the effects of SAM-e on pain and function may be potentially clinically relevant but are expected to be
small.[104]

Chondroprotective drugs (ie, matrix metalloproteinase [MMP] inhibitors and growth factors) are being tested as disease-
modifying drugs in the management of osteoarthritis. For example, MMP-13 is specifically expressed in the cartilage of
individuals with osteoarthritis but not in the cartilage of normal adults.[105] German researchers reported on the synthesis and
biologic evaluation of an MMP-13 selective inhibitor that has demonstrated efficacy as a disease-modifying intra-articular
injection for osteoarthritis.[106]

Other investigational agents include monoclonal antibodies that inhibit nerve growth factor (NGF), such as tanezumab. Anti-NGF
agents have been shown to reduce chronic pain in patients with osteoarthritis.[107, 108]

Lifestyle Modification, Physical/Occupational Therapy, and Other

Nonpharmacologic Measures
Lifestyle modification, particularly exercise and weight reduction, is a core component in the management of osteoarthritis.[109,
110]  

There is substantial evidence regarding the short-term benefits of therapy on pain and function, with long-term effectiveness
improved with adherence to home-based exercise programs. However, Bennell et al reported that in 74 patients with medial knee
osteoarthritis who completed a 12-week physiotherapist-supervised exercise trial, the addition of two 30-minute physiotherapy
booster sessions had no significant influence on pain, physical function outcomes, or measures of home exercise adherence.
[111]

Instruct the patient to avoid aggravating stress to the affected joint. Implement corrective procedures if the patient has poor
posture.

Weight reduction relieves stress on the affected knees or hips. The benefits of weight loss, whether obtained through regular
exercise and diet or through surgical intervention, may extend not only to symptom relief but also to a slowing in cartilage loss in
weight-bearing joints (eg, knees).[112] In addition, weight loss lowers levels of the inflammatory cytokines and adipokines that
may play a role in cartilage degradation.[113]

Some patients with osteoarthritis benefit from heat placed locally over the affected joint. A minority of patients report relief with
ice.[114]

In a study of 26 patients with painful and deforming hand osteoarthritis, rigid, custom splints worn nightly on one arthritic finger
joint per patient for three months significantly reduced pain in 17 of the 23 patients (74%) who completed the study. Average
pain remained significantly lower in splinted joints compared with non-splinted joints three months after patients stopped using
the splints.[115, 116]

Physical activity

Although people with osteoarthritis tend to avoid activity, exercise is an effective treatment for this condition, producing
improvements in pain, physical function, and walking distance. Long-term walking and resistance-training programs have been
shown to slow the functional decline seen in many patients with osteoarthritis, including older patients.[113]

In a systematic review and meta-analysis of 48 randomized controlled trials, Juhl and colleagues found that the optimal exercise
program for reducing pain and patient-reported disability in knee osteoarthritis should have a single aim, which can be improving
aerobic capacity, strengthening the quadriceps muscle, or improving lower extremity performance. For best results, the exercise
program should be supervised and performed 3 times weekly.[117]

Osteoarthritis of the knee may result in disuse atrophy of the quadriceps. Because these muscles help protect the articular
cartilage from further stress, quadriceps strengthening is likely to benefit patients with knee osteoarthritis. Stretching exercises
are also important in the treatment of osteoarthritis because they increase range of motion.
In a study of patients with knee osteoarthritis, Jan et al found that in most respects, non–weight-bearing exercise was as
therapeutically effective as weight-bearing exercise.[118] After an 8-week exercise program, the 2 types of exercise resulted in
equally significant improvements in function, walking speed, and muscle torque. However, patients in the weight-bearing group
demonstrated greater improvement in position sense, which may help patients with complex walking tasks, such as walking on
a spongy surface.

Chaipinyo and Karoonsupcharoen found no significant difference between home-based strength training and home-based
balance training for knee pain caused by osteoarthritis. However, greater improvement in knee-related quality of life was noted in
the strength-training group.[119]

The importance of aerobic conditioning, particularly low-impact exercises (if osteoarthritis is affecting weight-bearing joints),
should be stressed as well. Swimming, especially the aerobic aquatic programs developed by the Arthritis Foundation, can be
helpful.

The benefits of exercise have been found to decline over time, possibly because of poor adherence. Factors that determine
adherence to exercise have not been carefully studied in patients with osteoarthritis. In a review of this topic, Marks and
Allegrante concluded that interventions to enhance self-efficacy, social support, and skills in the long-term monitoring of
progress are necessary to foster exercise adherence in people with osteoarthritis.[120]

Tai chi

A prospective, single-blind, randomized, controlled study by Wang et al suggested that tai chi is a potentially effective treatment
for pain associated with osteoarthritis of the knee.[121] In this trial, 40 patients with symptomatic tibiofemoral osteoarthritis
who performed 60 minutes of tai chi twice weekly for 12 weeks experienced significantly greater pain reduction than did control
subjects who underwent 12 weeks of wellness education and stretching.

The mean difference in Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) pain scores was −118.80
mm.[121] The tai chi cohort also had significantly better WOMAC physical function scores, patient and physician global visual
analog scale scores, chair stand times, Center for Epidemiologic Studies Depression Scale scores, self-efficacy scores, and
Short Form 36 physical component summaries.

A subsequent trial by Wang et al that compared tai chi (2 times per week for 12 weeks) with standard physical therapy (2 times
per week for 6 weeks, followed by 6 weeks of monitored home exercise), reported substantial and comparable reductions in
WOMAC scores in both patient groups, as well as smilar clinically significant improvement in most secondary outcomes, and the
benefits were maintained up to 52 weeks. Furthermore, the tai chi group had significantly greater improvements in depression
and the physical component of quality of life.[122]

A systematic review and meta-analysis concluded that research results are encouraging and suggest that tai chi may be
effective in controlling pain and improving physical function in patients with knee osteoarthritis.[123] The researchers noted,
however, that the strength of the evidence is limited by the small number of randomized, controlled trials with a low risk of bias.

Assistive devices

The use of assistive devices for ambulation and for activities of daily living (ADLs) may be indicated for patients with
osteoarthritis. Braces  may also be of some use. A cane can be used in the contralateral hand for hip or knee osteoarthritis. The
patient can be taught joint-protection and energy-conservation techniques.

In a randomized study of 126 patients with painful knee osteoarthritis, wearing a slip-on knee brace for a median of 7.35 hours a
day for 6 weeks reduced pain and bone marrow lesions. Pain scores during activity declined about 18 points in patients using
the brace, but showed almost no change in those not wearing the brace. MRIs revealed that bone marrow lesion volumes in the
patellofemoral joint, which were nearly identical at baseline in both groups, had decreased by 25% after 6 weeks in patients in
the brace group.[124]

For patients with hand osteoarthritis, the ACR conditionally recommends evaluating the patient’s ability to perform ADLs and
providing assistive devices as needed. The ACR conditionally recommends splints for patients with trapeziometacarpal joint
involvement.[125]

For knee osteoarthritis, guidelines recommend appropriate footwear as part of self-management. However, a randomized trial
by Hinman et al that compared shoes designed to unload the knee versus new conventional shoes found that both groups
showed comparable improvement in pain with walking as well as other benefits. In the trial, the intervention group received
walking shoes with triple-density, variable-stiffness midsoles and mild lateral-wedge insoles designed to unload the medial knee
and worn daily, while the control group received supportive lace-up walking shoes.[126]

Occupational therapy and physical therapy

Occupational adjustments may be necessary for some patients with osteoarthritis. An occupational therapist can assist with
evaluating how well the patient performs ADLs, as well as with retraining of the patient as necessary. Joint-protection
techniques should be emphasized. Physical therapy modalities, especially those aimed at deconditioned patients, can be
helpful, particularly in patients with hip or knee involvement.

Electromagnetic field stimulation and TENS

A pulsed electromagnetic field stimulation device (Bionicare) has been approved by the US Food and Drug Administration (FDA)
for use in patients with knee osteoarthritis. Pulsed electromagnetic field stimulation is believed to act at the level of articular
cartilage by maintaining the proteoglycan composition of chondrocytes through downregulation of its turnover.[127]

A multicenter, double-blind, randomized, placebo-controlled 4-week trial in 78 patients with knee osteoarthritis found improved
pain and function in those who were treated with the device.[128] A double-blind, placebo-controlled 3-month trial in 58 patients
with moderate-to-severe knee osteoarthritis showed that the use of a highly optimized, capacitively coupled, pulsed electrical
stimulus device yielded significant symptomatic and functional improvement.[129]

Another randomized clinical trial demonstrated that pulsed short-wave treatment was effective in relieving pain and improving
function and quality of life in women with knee osteoarthritis on a short-term basis; additional studies are needed to validate the
12-month follow-up.[130]

Transcutaneous electrical nerve stimulation (TENS) may be another treatment option for pain relief. To date, however, there is
only limited evidence that TENS is beneficial in this setting. A systematic review could not confirm that TENS is effective for pain
relief in knee osteoarthritis.[131] A randomized controlled trial found that TENS applied in conjunction with therapeutic exercise
and daily activities increased quadriceps activation and function in patients with tibiofemoral osteoarthritis.[132]

Acupuncture

Acupuncture is becoming a more frequently used option for treatment of the pain and physical dysfunction associated with
osteoarthritis. Some evidence supports its use. For example, a review article of randomized, controlled trials reported that the
level of pain persisting after acupuncture was significantly lower than the level of pain persisting after control treatments.[133]

Several groups have issued guidelines regarding acupuncture for knee osteoarthritis. The AAOS does not recommend the use of
acupuncture for symptomatic knee osteoarthritis (strong recommendation).[134] The ACR recommends traditional Chinese
acupuncture for patients with chronic moderate-to-severe pain who would be candidates for total knee arthroplasty but who
either do not want it or have contraindications to it.[125]

Arthroscopy
A procedure of low invasiveness and morbidity, arthroscopy will not interfere with future surgery. However, a randomized,
controlled trial in patients with moderate-to-severe osteoarthritis found that arthroscopic surgery for osteoarthritis of the knee
provided no additional benefit beyond that afforded by optimized physical and medical therapy.[12]

Arthroscopy is indicated for removal of meniscal tears and loose bodies; less predictable arthroscopic procedures include
debridement of loose articular cartilage with a microfracture technique and cartilaginous implants in areas of eburnated
subchondral bone (see the images below). These treatments have varying success rates and should be performed only by
surgeons experienced in arthroscopic surgical techniques.[12, 135, 136] Overall, arthroscopy is not recommended for
nonspecific “cleaning of the knee” in osteoarthritis.
Arthroscopic view of a torn meniscus before (top) and after (bottom) removal of loose meniscal fragments.

Arthroscopic view of an arthritic knee.

Arthroscopic view of a knee after the removal of loose fragments of articular and meniscal cartilage.

Arthroscopic view of the removal of cartilaginous loose body.

Patients who undergo arthroscopy usually require a period of crutch use or exercise therapy. This period typically lasts days but
sometimes extends for weeks.

Osteotomy
Osteotomy is used in active patients younger than 60 years who have a malaligned hip or knee joint and want to continue with
reasonable physical activity.[137] The principle underlying this procedure is to shift weight from the damaged cartilage on the
medial aspect of the knee to the healthy lateral aspect of the knee. Osteotomy is most beneficial for significant genu varum, or
bowleg deformity. (The effectiveness of osteotomy for genu valgum is not highly predictable.)

Osteotomy often can help individuals avoid requiring a total knee replacement until they are older. It can lessen pain, but it can
also lead to more challenging surgery if the patient later requires arthroplasty.
A follow-up study of 147 opening-wedge high tibial osteotomies in a consecutive series of patients affected by varus knee
malalignment with isolated medial compartment degenerative joint disease reported good or excellent results in 94% of cases.
Follow-up averaged 9.5 years, with a range of 7 to 12 years.[138]

Contraindications for osteotomy are as follows:

Knee flexion of less than 90°

A flexion-extension contracture of more than 15°
Varus over 15°-20°
Instability from previous trauma or surgery
Severe arterial insufficiency
Bicompartmental involvement

Patients undergoing osteotomy require partial weight-bearing until bony healing occurs. Afterward, exercise is indicated.

Arthroplasty
Arthroplasty consists of the surgical removal of joint surface and the insertion of a metal and plastic prosthesis (see the images
below). The prosthesis is held in place by cement or by bone ingrowth into a porous coating on the prosthesis. The use of
cement results in faster pain relief, but bone ingrowth may provide a more durable bond; accordingly, prostheses with a porous
coating are used in younger patients.

Anteroposterior radiograph shows knee replacement in 1 knee and arthritis in the other, with medial joint-space narrowing and
subchondral sclerosis.

Anteroposterior radiograph of the pelvis and hips shows an arthritic hip not treated surgically and a total hip replacement.
Anteroposterior radiograph obtained after knee replacement.

Lateral radiograph obtained after knee replacement (same patient as in the above image).

Arthroplasty is performed if all other modalities are ineffective and osteotomy is not appropriate or if a patient cannot perform
ADLs despite maximal therapy.[139, 140] This procedure alleviates pain and may improve function. At a minimum, 10-15 years
of viability are expected from joint replacement in the absence of complications.

Infection is a particular postoperative concern in cases of total joint replacement. This complication is now rare, however,
especially with the use of perioperative antibiotics.
Prevention of thrombophlebitis and resultant pulmonary embolism is important in patients who undergo lower-extremity
arthroplasty procedures for osteoarthritis. The surgeon must use all means available to prevent these complications. Early
motion and ambulation, when possible, are of particular importance. The use of low-molecular-weight heparin or warfarin is also
indicated.

After joint replacement, patients require partial weight-bearing, which progresses to full weight-bearing in 1-3 months; range-of-
motion and strengthening exercises are started within a few days after joint-replacement surgery and continued until the patient
has good range of motion and strength. After resection arthroplasty of the hip, patients require instruction in the use of crutches
or a walker, which are usually needed permanently.

For more information, see the following articles:

Total Knee Arthroplasty

Unicompartmental Knee Arthroplasty

Surgical Treatment of Interphalangeal Joint Arthritis

Minimally Invasive Total Hip Arthroplasty

Fusion and Joint Lavage

Fusion consists of the union of bones on either side of the joint. This procedure relieves pain but prevents motion and puts more
stress on surrounding joints. Fusion is sometimes used after knee replacements fail or as a primary procedure for ankle or foot
arthritis.

Observational studies suggested a benefit for joint lavage. However, sham-controlled trials yielded conflicting results, and a
meta-analysis concluded that joint lavage does not result in pain relief or improvement of function in patients with knee
osteoarthritis.[141]

Prevention
Overweight patients who have early signs of osteoarthritis or who are at high risk should be encouraged to lose weight.
Recommend quadriceps-strengthening exercises in patients with osteoarthritis of the knees, except in those with pronounced
valgus or varus deformity at the knees. (See Lifestyle Modification, Physical/Occupational Therapy, and Other
Nonpharmacologic Measures.)

It has been proposed that low vitamin D levels may play a role in the development and progression of osteoarthritis; however,
studies of vitamin D status and osteoarthritis have produced conflicting results.[142, 143]

A systematic review found no convincing evidence that selenium, vitamin A, or vitamin C is effective for the treatment of
osteoarthritis.[144] A prospective cohort study also found no evidence that vitamin C supplementation slowed the progression
of knee osteoarthritis; however, it did find that patients who reported taking vitamin C were 11% less likely to develop knee
osteoarthritis.[145]

Stem Cell Therapy

Mesenchymal stem cells (MSCs) are an investigational treatment of osteoarthritis. The International Society for Cellular Therapy
(ISCT) defines MSC to be mesenchymal “stromal” cells having the attributes of being plastic-adherent culture-expanded cells
without hematopoietic cell markers that express specific cell surface markers (ie, CD73, CD90, and CD105) and that show the
ability to differentiate into osteoblasts, adipocytes, and chondrocytes in vitro.[100]  In clinical trials, placement of MSCs into the
knee joint has proved an effective treatment for osteoarthritis.[74, 75, 11, 146]  However, no MSC therapies have yet been
cleared by the FDA for human clinical application to musculoskeletal diseases.[100]
MSCs can be derived from a variety of tissues, but for therapeutic purposes they are collected from bone marrow or adipose
tissue. They can differentiate into a variety of cell types, secrete bioactive molecules that stimulate angiogenesis and tissue
repair, and reduce T-cell response and inflammation. Autologous MSCs are easily harvested and used therapeutically, but
allogenic MSCs have been utilized. Delivery methods have included implantation and microfracture, but the current focus is on
intra-articular injection of suspensions containing large numbers of cells.[74, 75]

A meta-analysis comparing the conditions of patients with knee osteoarthritis before and after treatment with MSCs
demonstrated continual efficacy for at least 24 months, with greater pooled effect size (pain and functional changes) at 12 and
24 months than summed effect sizes at 3 months. However, a dose-responsiveness association was not demonstrated in the
MSC numbers. Notably, MSC therapy appeared more beneficial in patients with early osteoarthritis than in those with advanced
disease.[74]

Two systematic reviews have questioned the quality of the studies of stem cell therapy for knee osteoarthritis, citing high risk of
bias, low quality of evidence, only modest improvement reported, and possible placebo effect.[76, 77]  Nevertheless, a survey
identified hundreds of clinics in the United States that offer stem cell therapy for knee arthritis, at prices ranging from $1150 to
$12,000 for a unilateral injection. In many cases these injections would consist of centrifuged blood or bone marrow aspirate
rather than cultivated stem cells.[147]  

Guidelines

Guidelines Summary
Guidelines on osteoarthritis have been issued by the following organizations:

American College of Rheumatology (ACR) – Nonpharmacologic and pharmacologic therapies for hand, hip, and knee
osteoarthritis
Osteoarthritis Research Society International (OARSI) – Nonpharmacologic therapies for hip and knee osteoarthritis
American Academy of Orthopaedic Surgeons (AAOS) – 1) Nonpharmacologic and pharmacologic therapies and joint
replacement for knee osteoarthritis; 2) Surgical management of osteoarthritis of the knee; 3) Management of
osteoarthritis of the hip

Hand Osteoarthritis
For hand osteoarthritis, the American College of Rheumatology (ACR) conditionally recommends the following[125] :

Evaluate the ability to perform activities of daily living (ADLs)

Instruct in joint protection techniques
Provide assistive devices, as needed, to help patients perform ADLs
Instruct in use of thermal modalities
Provide splints for patients with trapeziometacarpal joint osteoarthritis

The ACR made no strong recommendations for the nonpharmacologic management of hand osteoarthritis, as the evidence
supporting those interventions demonstrated only minor to moderate benefits. For pharmacologic treatment, the ACR
conditionally recommends using one or more of the following[125] :

Topical capsaicin
Topical nonsteroidal anti-inflammatory drugs (NSAIDs), including trolamine salicylate
Oral NSAIDs
Tramadol

The ACR conditionally recommends against using intra-articular therapies or opioid analgesics for hand osteoarthritis. For
patients 75 years and older, the ACR conditionally recommends the use of topical rather than oral NSAIDs.
Knee Osteoarthritis
The Osteoarthritis Research Society International (OARSI) guidelines provides separate recommendations for treatment of
symptomatic arthritis in one or both knees (knee-only OA) and in the knee(s) in addition to other joints (e.g., hip, hand, spine,
etc). Separate recommendations are made based on the absence or presence of comorbidities (ie, diabetes; hypertension; CV
disease; renal failure; gastrointestinal (GI) bleeding; depression; or physical impairment limiting activity, including obesity). The
following nonpharmacologic recommendations apply to all subphenotypes[72] :

Biomechanical interventions such as knee braces, knee sleeves, and foot orthoses as directed by an appropriate
specialist
Land-based exercise and strength training
Aquatic exercise
Self-management and education
Weight management

The OARSI recommmends use of a cane in knee-only OA to diminish pain and improve function and some aspects of quality of
life. However, there was a lack of evidence for benefit  in mutiple-joint OA. The guidelines noted that cane use could be
inappropriate for some patients because to relief of knee pain may require an increase in the weight-bearing load on other
affected joints (e.g., contralateral hand and hip joints).[72]

For multiple-joint OA with comorbidities, balneotherapy (defined as the use of baths containing thermal mineral waters) is
recommended and includes practices such as Dead Sea salt or mineral baths, sulfur baths, and radon-carbon dioxide baths.[72]  

The American College of Rheumatology (ACR) strongly recommends the following nonpharmacologic measures for patients
with knee osteoarthritis[125] :

Cardiovascular (aerobic) and/or resistance land-based exercise

Aquatic exercise
Weight loss for overweight patients

The ACR conditionally recommends the following nonpharmacologic measures for patients with knee osteoarthritis:

Self-management programs
Manual therapy in combination with supervised exercise
Psychosocial interventions
Medially directed patellar taping
Medially wedged insoles for lateral-compartment osteoarthritis
Laterally wedged subtalar strapped insoles for medial-compartment osteoarthritis
Thermal agents
Walking aids, as needed
Tai chi

The ACR has no recommendations regarding the following:

Balance exercises, either alone or in combination with strengthening exercises

Laterally wedged insoles
Manual therapy alone
Knee braces
Laterally directed patellar taping

An American Academy of Orthopaedic Surgeons (AAOS) guideline suggests encouraging patients with knee osteoarthritis to
participate in self-management educational programs such as those conducted by the Arthritis Foundation and to incorporate
activity modifications into their lifestyle (eg, walking instead of running or engaging in alternative activities).

Acupuncture for knee osteoarthritis

Guidelines from different groups offer a range of recommendations regarding the use of acupuncture for knee osteoarthritis, as
follows:

The ACR conditionally recommends traditional Chinese acupuncture for patients with chronic moderate-to-severe pain
who would be candidates for total knee arthroplasty but who either do not want it or have contraindications to it. [125]
The OARSI guidelines find the efficacy of acupuncture to be uncertain. [72]
The AAOS strongly recommends against the use of acupuncture for symptomatic knee osteoarthritis. [134]

Pharmacologic therapy
The OARSI recommmends intra-articular corticosteroid injections and oral nonselective NSAIDS for treatment of all
subphenotypes. COX-2 selective oral NSAIDs were deemed apporpriate for individulals without comorbidities and mutiple-joint
OA with moderate co-morbidity risk. Proton-pump inhibitor (PPI) co-prescription with oral NSAIDs is not recommended for those
with no co-morbidity risk. For those with moderate or high co-morbidity risk receiving oral non-selective NSAIDs, PPI co-
prescription is recommended. No recommendation was made for individuals taking  COX-2 selective oral NSAIDs at moderate
mobidy risk. Use of oral NSAIDs is stongly advised against for individuals with high co-morbidity risk.[72]  

Duloxetine is recommended for most subphenotypes, however, associated adverse events and availability of more targeted
therapies predicated uncertain appropriateness for individuals with knee-only OA and co-morbidities.[72]

Additional recommendations include[72] :

Acetaminophen for patients without co-morbidities

Topical capsaicin for knee-only OA without co-morbidities; uncertain for multiple-joint OA and in patients with co-
morbidities
Topical NSAIDs for knee-only OA

For knee osteoarthritis, the ACR conditionally recommends using one of the following: 

Acetaminophen
Oral NSAIDs
Topical NSAIDs
Tramadol
Intra-articular corticosteroid injections

The ACR conditionally recommends against using chondroitin sulfate, glucosamine, or topical capsaicin for knee osteoarthritis.
The ACR has no recommendations regarding the use of intra-articular hyaluronates, duloxetine, and opioid analgesics.

American Academy of Orthopaedic Surgeons guidelines

A 2013 clinical practice guideline from the American Academy of Orthopaedic Surgeons (AAOS) recommends the following
pharmacologic treatments for symptomatic osteoarthritis of the knee[134] :

Oral NSAIDs
Topical NSAIDs
Tramadol

The AAOS was unable to recommend for or against the use of the following for symptomatic knee osteoarthritis:

Acetaminophen
Opioids
Pain patches
Intra-articular corticosteroid injections
Growth factor injections and/or platelet rich plasma

The recommendation on acetaminophen is a downgrade from the previous AAOS guideline, and reflects the use of new criteria
that resulted in the selection of only one study, which found no statistical significance or minimum clinically important
improvement with acetaminophen compared with placebo.

The AAOS does not recommend treatment with any of the following:

Intra-articular hyaluronic acid

Glucosamine and/or chondroitin sulfate or hydrochloride

Knee replacement

A 2016 guideline on surgical management of knee osteoarthritis from the American Academy of Orthopaedic Surgeons (AAOS)
includes the following recommendations regarding total knee arthroplasty (TKA)[148] :

Obese patients have less improvement in outcomes (strong supporting evidence)

Patients with diabetes are at higher risk for complications (moderate evidence)
Patients with select chronic pain conditions have less improvement in patient-reported outcomes (moderate)
Patients with depression and/or anxiety symptoms have less improvement in patient-reported outcomes (limited)
Patients with cirrhosis or hepatitis C are at higher risk for complications (limited)
An 8-month delay to TKA does not worsen outcomes (moderate)
Supervised exercise before TKA might improve pain and physical function after surgery (limited)
Compared with placebo, peri-articular local anesthetic infiltration in TKA decreases pain and opioid use (strong)
 Compared with general anesthesia, neuraxial anesthesia can improve select perioperative outcomes and complication
rates (moderate)
Use of a tourniquet in TKA decreases intraoperative blood loss (moderate) but increases short-term postoperative pain
(strong) and decreases short- term postoperative function (limited)
In patients with no known contraindications, treatment with tranexamic acid decreases postoperative blood loss and
reduces the necessity of postoperative transfusions (strong)
Routine use of antibiotics in the cement for primary TKA is not recommended (limited)
Outcomes and complications are no different with posterior-stabilized versus posterior cruciate–retaining arthroplasty
designs
Outcomes are no different with either all-polyethylene or modular tibial components (strong)
Use of patellar resurfacing makes no difference in pain or function (strong), but could decrease cumulative reoperations
after 5 years (moderate)
Cemented or cementless tibial component fixation provides similar functional outcomes and rates of complications and
reoperations (strong)
Use of either cemented or cementless femoral and tibial components results in similar rates of complications and
reoperations (moderate)
Either cementing all components or using hybrid fixation (cementless femur) results in similar functional outcomes and
rates of complications and reoperations. (moderate)
Use of either all cementless components or hybrid fixation (cementless femur) results in similar rates of complications
and reoperations (limited)
Simultaneous bilateral TKA can be performed in patients aged 70 or younger or with American Society of
Anesthesiologists (ASA) status 1-2, because there are no increased complications (limited)
In patients with medial compartment osteoarthritis, revision surgery risk could be lower with TKA than with (moderate);
however, risk of deep venous thrombosis and manipulation under anesthesia may be higher with TKA) than with
unicompartmental knee arthroplasty (limited)
In patients with medial compartment knee osteoarthritis, there is no difference in outcome and complications with
unicompartmental knee arthroplasty versus valgus-producing proximal tibial osteotomy (moderate)
Using intraoperative navigation makes no difference in outcomes or complications (strong)
Compared with conventional instrumentation, use of patient-specific instrumentation for TKA makes no difference in
pain or functional outcomes (strong) or in transfusions or complications (moderate)
Use of a drain with TKA makes no difference in complications or outcomes (strong)
Use of cryotherapy devices after TKA does not improve outcomes (moderate)
Postoperative continuous passive motion (CPM) does not improve outcomes (strong)
Rehabilitation started on the day of surgery reduces length of hospital stay (strong), and reduces pain and improves
function compared with rehabilitation started on postoperative day 1 (moderate)
A supervised exercise program during the first 2 months after TKA improves physical function (moderate) and may
decrease pain (limited)
Selected patients might be referred to an intensive supervised exercise program during late-stage post-TKA to improve
physical function (limited)

Hip Osteoarthritis
The American College of Rheumatology (ACR) strongly recommends the following nonpharmacologic measures for patients
with hip osteoarthritis[125] :

Cardiovascular and/or resistance land-based exercise

Aquatic exercise
Weight loss, for overweight patients

The ACR conditionally recommends the following nonpharmacologic measures for patients with hip osteoarthritis:

Self-management programs
Manual therapy in combination with supervised exercise
Psychosocial interventions
Thermal agents
Walking aids, as needed

The ACR conditionally recommends using one or more of the following pharmacologic agents for initial management of hip
arthritis:

Acetaminophen
 Oral NSAIDs
Tramadol
Intra-articular corticosteroid injections

The ACR conditionally recommends against using chondroitin sulfate or glucosamine for hip osteoarthritis. The ACR has no
recommendation regarding the use of topical NSAIDs, intra-articular hyaluronate injections, duloxetine, or opioid analgesics.

A 2017 guideline on management of hip osteoarthritis from the American Academy of Orthopaedic Surgeons (AAOS) place an
emphasis on presurgical treatments to reduce pain and increase mobility and also highlight patient populations who may have
greater risk associated with hip replacement surgery.[149] The guidelines found moderate strength evidence for the following
risk issues[150] :

Practitioners may use risk assessment tools for predicting complications, assessing surgical risks, and educating
patients about receiving total hip arthroplasty.

Obese patients may have lower absolute outcome scores, but similar levels of satisfaction and improvement in pain and
function after total hip replacement compared with nonobese patients.

Increased age is associated with lower functional and quality-of-life outcomes after total hip replacement.

Mental health disorders, including depression, anxiety, and psychosis, are associated with decreased function, pain relief,
and quality of life after total hip replacement.

The AAOS found strong evidence regarding the following management approaches[150] :

Nonnarcotic medications: Nonsteroidal anti-inflammatory drugs (NSAIDs) improve short-term pain, function, or both.

Corticosteroid injections provide short-term improvements in function and pain.

Hyaluronic acid injections are no better than placebo for improving function, stiffness, and pain.

Physical therapy improves function and decreases pain in mild to moderate hip osteoarthritis.

There was moderate strength evidence for the following[150] :

Postoperative physical therapy improves early function more than no physical therapy.

Glucosamine sulfate is no better than placebo for improving function, reducing stiffness, and decreasing pain.

Practitioners may use intravenous or topical tranexamic acid to reduce blood loss associated with total hip replacement
surgery.

No clinically significant differences in patient-oriented outcomes for anterior vs posterior approaches in total hip
replacement.

Medication

Medication Summary
The goals of pharmacotherapy in osteoarthritis are to reduce morbidity and to prevent complications. To date, no disease-
modifying or structure-modifying intervention has been proved effective in osteoarthritis. Pay careful attention to a particular
pharmacologic regimen’s adverse-event profile.

Pharmacologic agents used in the treatment of osteoarthritis include the following:

Acetaminophen
Nonsteroidal anti-inflammatory drugs (NSAIDs), oral and topical (eg, diclofenac topical [151] )
Calcium channel blocker/COX-2 inhibitor combination
Intra-articular corticosteroids
Intra-articular sodium hyaluronate
Opioids
Duloxetine
Muscle relaxants
 Nutraceuticals (eg, glucosamine/chondroitin sulfate)

Analgesics, Other

Class Summary
Pain control is essential to the management of osteoarthritis. The goals of treatment include pain alleviation and improvement
of functional status.

Acetaminophen (Tylenol)
An initial trial with acetaminophen is warranted in patients with mild-to-moderate osteoarthritis symptoms who do not derive
sufficient relief from nonpharmacologic measures. Acetaminophen is the drug of choice for patients who have a documented
hypersensitivity to aspirin or NSAIDs, who have a history of upper gastrointestinal (GI) tract disease, or who are on
anticoagulants.

Nonsteroidal Anti-inflammatory Drugs (NSAIDs)

Class Summary
NSAIDs have analgesic, anti-inflammatory, and antipyretic activities. They are used to relieve osteoarthritis pain when the clinical
response to acetaminophen is unsatisfactory. The mechanism of action is nonselective inhibition of cyclooxygenase (COX)-1
and COX-2, resulting in reduced synthesis of prostaglandins and thromboxanes. Other mechanisms may also exist, such as
inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell-
membrane functions.

In more inflammatory presentations of osteoarthritis, such as knee involvement with effusion, these agents may be used as
first-line pharmacologic therapy. Use the lowest effective dose or intermittent therapy if symptoms are intermittent. All of these
medications increase the risk for GI ulcers and have been associated with increased risk of cardiovascular disease. Patients at
high risk for GI toxicity may consider adding misoprostol or a proton-pump inhibitor to the regimen or substituting a COX-2–
specific inhibitor for the NSAID.

The FDA approved a submicron low-dose product (Zorvolex) for osteoarthritis that allows treatment at a lower dose than the
diclofenac sodium and potassium salts. Submicron diclofenac 35 mg PO TID significantly improved Western Ontario and
McMasters Universities Osteoarthritis Index (WOMAC) pain subscale scores from baseline at 12 weeks (-44.1; p = 0.0024)
compared with placebo (-32.5).[152]

Ketoprofen
Ketoprofen is indicated for relief of mild-to-moderate pain and inflammation. Small dosages are initially indicated in small and
elderly patients and in those with renal or liver disease. Doses higher than 75 mg do not increase therapeutic effects. Administer
high doses with caution, and closely observe the patient for response.

Piroxicam (Feldene)
Piroxicam decreases the activity of cyclooxygenase, which in turn inhibits prostaglandin synthesis. These effects decrease
formation of inflammatory mediators.

Ibuprofen (Advil, Motrin IB, Caldolor, Neoprofen)

Ibuprofen relieves pain and inflammation. It is widely available and is relatively inexpensive as a generic drug. After the very early
stages of osteoarthritis, inflammation begins to play a role in the disease. Thus, medications with a combination of analgesic
and anti-inflammatory properties become more desirable, at least in theory.

Meloxicam (Mobic)
To some extent, meloxicam is more selective for COX-2 receptors than traditional NSAIDs are. It decreases the activity of
cyclooxygenase, thereby, in turn, inhibiting prostaglandin synthesis. These effects decrease the formation of inflammatory
mediators.

Diclofenac (Voltaren XR, Cataflam, Cambia, Zipsor)

Diclofenac is one of a series of phenylacetic acids that have demonstrated anti-inflammatory and analgesic properties in
pharmacologic studies. It is believed to inhibit cyclooxygenase, which is essential in the biosynthesis of prostaglandins.
Diclofenac can cause hepatotoxicity; hence, liver enzymes should be monitored in the first 8 weeks of treatment.

Diclofenac is rapidly absorbed; metabolism occurs in the liver by demethylation, deacetylation, and glucuronide conjugation. The
delayed-release, enteric-coated form is diclofenac sodium, and the immediate-release form is diclofenac potassium. It poses a
relatively low risk for bleeding GI ulcers.

Celecoxib (Celebrex)
Celecoxib is a COX-2–specific inhibitor. At therapeutic concentrations, COX-2 (inducible by cytokines at sites of inflammation,
such as the joints) is inhibited, and COX-1 isoenzyme (present in platelets and the GI tract) is spared; therefore, in nonaspirin
users, the incidence of GI toxicity (eg, endoscopic peptic ulcers, bleeding ulcers, perforations, and obstructions) is decreased in
comparison with that seen in patients taking nonselective NSAIDs.

Naproxen (Aleve, Anaprox, Anaprox DS, Naprelan, Naprosyn)

Naproxen is used for relief of mild to moderate pain. It inhibits inflammatory reactions and pain by decreasing the activity of
cyclooxygenase, which is responsible for prostaglandin synthesis. NSAIDs decrease intraglomerular pressure and decrease
proteinuria.

Calcium Channel Blocker/COX-2 Inhibitor Combination

Class Summary
This combination provides blood pressure lowering affect from amlodipine to reduce the risk of fatal and nonfatal CV events,
primarily strokes and myocardial infarctions.

Celecoxib/amlodipine (Consensi)
Celecoxib inhibits cyclooxygenase (COX)-2 which decreases formation of prostaglandin synthesis. Elicits analgesic, anti-
inflammatory, and antipyretic properties. Amlodipine, a calcium channel blocker, Inhibits transmembrane influx of extracellular
calcium ions across membranes of myocardial cells and vascular smooth muscle cells without changing serum calcium
concentrations; this inhibits cardiac and vascular smooth muscle contraction, thereby dilating main coronary and systemic
arteries. In clinical trials, the combination lowered diastolic and systolic blood pressure (both daytime and nighttime
measurements) similarly to an equal dose of amlodipine. It is indicated in adults for whom treatment with both amlodipine for
hypertension and celecoxib for osteoarthritis are appropriate.

Antidepressants, SNRIs
Class Summary
The selective serotonin-norepinephrine reuptake inhibitor (SNRI) duloxetine may be effective for reducing osteoarthritis pain.

Duloxetine (Cymbalta)
Potent inhibitor of neuronal serotonin and norepinephrine reuptake. Indicated for chronic musculoskeletal pain, including
discomfort from osteoarthritis and chronic lower back pain.

Analgesic, Topical

Class Summary
Topical analgesics are used for osteoarthritis involving relatively superficial joints, such as the knee joint and the joints of the
hands. They are much less effective for deeper joints, such as the hip joint.

Capsaicin (Qutenza)
Capsaicin is a topical analgesic of choice in osteoarthritis. Derived from plants of the Solanaceae family, it may render skin and
joints insensitive to pain by depleting substance P in peripheral sensory neurons. Capsaicin must be used for at least 2 weeks
for the full effects to be appreciated.

Opioid Analgesics

Class Summary
Opioid analgesics are used in patients whose pain has not been controlled with weaker analgesic medications. They are a
particularly reasonable choice in patients who do not want joint-replacement surgery, are too medically ill for joint replacement,
are not candidates for joint replacement for other reasons, or are trying to buy time for subsequent joint-replacement surgery.

Elderly patients (aged 65 years and older) with arthritis are more likely to incur a fracture when initiating opioid therapy as
opposed to NSAID therapy. A higher opioid dose is associated with a greater risk of fracture; this risk is due to an increased risk
of falls. During the first 2 weeks after initiation of opioid treatment, short-acting opioids are associated with a greater fracture
risk than long-acting opioids are.[153]

Tramadol (Ultram, Ultram ER, ConZip)

Tramadol inhibits ascending pain pathways, altering perception of and response to pain. This agent also inhibits the reuptake of
norepinephrine and serotonin.

Oxycodone (OxyContin, Roxicodone)

Pure narcotic analgesics, such as oxycodone, might be the initial drug of choice. Eventually, this short-acting narcotic can be
replaced with a long-acting transdermal preparation, such as fentanyl (Duragesic patch).
Corticosteroids

Class Summary
Intra-articular pharmacologic therapy includes corticosteroid injection and viscosupplementation. Steroid injections generally
result in a clinically and statistically significant reduction in osteoarthritic knee pain as soon as 1 week after injection. The effect
may last, on average, anywhere from 4 to 6 weeks per injection, but the benefit is unlikely to continue beyond that time frame.
However, triamcinolone acetonide extended-release injectable suspension (Zilretta) may reduce pain intensity for up to 12
weeks.

Triamcinolone acetonide extended-release injectable suspension (Zilretta)

Corticosteroid with anti-inflammatory and immunomodulating properties. It binds to and activates the glucocorticoid receptor,
leading to activation of anti-inflammatory transcription factors (eg, lipocortins). It also inhibits inflammatory transduction
pathways by blocking arachidonic acid release and preventing prostaglandin and leukotriene synthesis. Indicated for
management of osteoarthritis knee pain. Administered as a single intra-articular injection. Not intended for repeat
administration.

Triamcinolone acetonide injectable suspension (Kenalog-40)

Corticosteroid with anti-inflammatory and immunomodulating properties; it binds to and activates the glucocorticoid receptor,
leading to activation of anti-inflammatory transcription factors (eg, lipocortins); it also inhibits inflammatory transduction
pathways by blocking arachidonic acid release and preventing prostaglandin and leukotriene synthesis. Indicated for intra-
articular injection for pain management of osteoarthritis.

Methylprednisolone (Depo-Medrol, Medrol, Solu-Medrol, A-Methapred)

Methylprednisolone decreases inflammation by suppressing migration of polymorphonuclear leukocytes (PMNs) and reversing
increased capillary permeability.

Betamethasone (Celestone Soluspan)

Betamethasone decreases inflammation by suppressing migration of PMNs and reversing increased capillary permeability. It
affects the production of lymphokines and has an inhibitory effect on Langerhans cells.

Antirrheumatic, Miscellaneous

Class Summary
Intra-articular injections of these agents are used to treat patients with osteoarthritic knee pain that is unresponsive to
conservative nonpharmacologic therapy and simple analgesics (eg, acetaminophen).

Sodium hyaluronate (Euflexxa, Hyalgan, Orthovisc, Supartz, Synvisc, Synvisc-One)

Sodium hyaluronate is a biological polysaccharide that supports the lubricating and shock-absorbing properties of articular
cartilage.

Skeletal muscle relaxants

Class Summary
The use of certain skeletal muscle relaxants have been shown to be helpful in osteoarthritis.

Carisoprodol (Soma)
Short-acting medication that may have depressant effects at spinal cord level.

Skeletal muscle relaxants have modest short-term benefit as adjunctive therapy for nociceptive pain associated with muscle
strains and, used intermittently, for diffuse and certain regional chronic pain syndromes. Long-term improvement over placebo
has not been established.

Dantrolene (Dantium, Revonto)

Acts peripherally at muscle fiber rather than at neural level; reduces muscle action potential–induced release of calcium and
also affects intrafusal and extrafusal fibers and spindle sensitivity. Has no action on smooth or cardiac muscle tissue. Induces
release of Ca++ into sarcoplasmic reticulum, subsequently decreasing the force of excitation coupling. Only drug that intervenes
at a muscular level. Preferred for the cerebral form of spasticity. Less likely to cause lethargy or cognitive changes like baclofen
or diazepam.

May reduce painful cramping and detrimental muscle tightening.

Can be administered PO/IV. IV form is much more expensive and should be reserved for patients unable to take oral
medications. Most patients respond to 400 mg/day or less. Eliminated in the urine and bile.

Baclofen (Lioresal)
Muscle relaxant (central), presynaptic GABA-B receptor agonist that may induce hyperpolarization of afferent terminals and
inhibit both monosynaptic and polysynaptic reflexes at spinal level. Lessens flexor spasticity and hyperactive stretch reflexes of
upper motor neuron origin. Eliminated through renal excretion.

Well absorbed, with average oral bioavailability of 60% and mean elimination half-life of 12 h; steady state reached within 5 d
with multiple dose administration; metabolism occurs in liver (P 450-dependent glucuronidation and hydroxylation); 6 major and
a few minor metabolites produced.

Questions & Answers

Overview

What is osteoarthritis (OA)?

What are the symptoms of osteoarthritis (OA)?

What are symptoms of osteoarthritis (OA) of the hand?

How is osteoarthritis (OA) diagnosed?

What is the role of imaging studies in the diagnosis of osteoarthritis (OA)?

Which arthrocentesis findings are characteristic of osteoarthritis (OA)?

What are the nonpharmacologic treatment options for osteoarthritis (OA)?

What are the American College of Rheumatology (ACR) recommendations for the treatment of osteoarthritis (OA) of the hand?

What are the American College of Rheumatology (ACR) recommendations for the treatment of osteoarthritis (OA) of the knee?

What are the American College of Rheumatology (ACR) recommendations for the treatment of osteoarthritis (OA) of the knee?

Which surgical procedures may be used in the treatment of osteoarthritis (OA)?

What is osteoarthritis (OA)?

What are the causes of osteoarthritis (OA)?

What is secondary osteoarthritis (OA)?

What is primary osteoarthritis (OA)?

How is osteoarthritis (OA) diagnosed?

What are the nonpharmacologic interventions for the treatment of osteoarthritis (OA)?

What are the pharmacologic therapy options for osteoarthritis (OA)?

When should NSAIDS be considered in the treatment of osteoarthritis (OA)?

What is the economic burden of osteoarthritis (OA)?

What is the functional classifications of joint movement in osteoarthritis (OA)?

What are the structural classifications of joint movement in osteoarthritis (OA)?

What is the anatomy of synovial joints involved in osteoarthritis (OA)?

What is the importance of synovial fluid in osteoarthritis (OA)?

What is the pathophysiology of osteoarthritis (OA)?

What is the role of inflammation in the pathogenesis of osteoarthritis (OA)?

Which inflammatory molecules are associated with osteoarthritis (OA)?

What is the pathogenesis of early osteoarthritis (OA)?

What is the pathogenesis of disease progression in osteoarthritis (OA)?

What is the role of joint space loss in the pathogenesis of osteoarthritis (OA)?

What is the role of eburnation in the pathogenesis of osteoarthritis (OA)?

How do cysts form in the pathogenesis of osteoarthritis (OA)?

What causes osteophytes to form during the pathogenesis of osteoarthritis (OA)?

Which neuromuscular abnormalities may result from osteoarthritis (OA)?

Which mechanisms are responsible for the perception of pain in osteoarthritis (OA)?

What are the signs and symptoms of osteoarthritis (OA) in the lumbar spine?

How does osteoarthritis (OA) develop?

What are the risk factors for osteoarthritis (OA)?

What is the role of aging in the etiology of osteoarthritis (OA)?

What is the role of obesity in the etiology of osteoarthritis (OA)?

What is the role of trauma or surgery in the etiology of osteoarthritis (OA)?

What is the role of muscle dysfunction in the etiology of osteoarthritis (OA)?

What is the role of valgus malalignment in the etiology of osteoarthritis (OA)?

What is the role of genetics in the etiology of osteoarthritis (OA)?

Which genes may be involved in the etiology of osteoarthritis?

What is the role of signaling cascades in the etiology of osteoarthritis (OA)?

Which genes have genome-wide association studies (GWAS) identified as having an etiologic role in osteoarthritis (OA)?

What is the importance of genetic factors in osteoarthritis (OA)?

What is the role of genetic testing in patients with osteoarthritis (OA)?

What is the prevalence of osteoarthritis (OA) in the US?

What is the global prevalence of osteoarthritis (OA)?

How does the prevalence of osteoarthritis (OA) vary by age?

How does the prevalence of osteoarthritis (OA) vary by sex?

How does the prevalence of osteoarthritis (OA) vary among racial groups?

What is the prognosis of osteoarthritis (OA)?

Which factors are associated with more rapid progression of knee osteoarthritis (OA)?

What is the prognosis of osteoarthritis in patients who have undergone joint replacement?

What information about osteoarthritis (OA) should patients receive?

Presentation

How is the progression of osteoarthritis (OA) characterized?

What is the presentation of early stage osteoarthritis (OA)?

What are the initial signs and symptoms of osteoarthritis (OA)?

Which physical findings suggest osteoarthritis (OA)?

Which physical findings suggest hand osteoarthritis (OA)?

What are the three stages of osteoarthritis (OA) pathogenesis?

What is the role of grading systems in the management of osteoarthritis (OA)?

Which diseases are categorized as subsets of primary osteoarthritis (OA)?

What are the classifications of hand osteoarthritis (OA)?

DDX

What is the initial diagnostic goal of the evaluation for osteoarthritis (OA)?

How is rheumatoid arthritis (RA) differentiated from osteoarthritis (OA)?

Which lab tests are used to differentiate rheumatoid arthritis (RA) from osteoarthritis (OA)?

How is spondyloarthropathy differentiated from osteoarthritis (OA)?

Which medical conditions may cause secondary osteoarthritis (OA)?

Which disorders should be included in the differential diagnoses of osteoarthritis (OA)?

What are the differential diagnoses for Osteoarthritis?

Workup

How is osteoarthritis (OA) diagnosed?

What are biomarkers for the diagnosis of osteoarthritis?

What is the role of lab testing in the evaluation of osteoarthritis (OA)?

What is the role of radiography in the diagnosis of osteoarthritis (OA)?

Which radiographic findings are characteristic of osteoarthritis (OA of the elbow?

What is the role of MRI in the diagnosis of osteoarthritis (OA)?

What is the role of CT scanning in the diagnosis of osteoarthritis (OA)?

What is the role of ultrasonography in the diagnosis of osteoarthritis (OA)?

What is the role of bone scanning in the diagnosis of osteoarthritis (OA)?

What is the role of arthrocentesis in the diagnosis of osteoarthritis (OA)?

Treatment

What are the goals of osteoarthritis (OA) treatment?

What are the nonpharmacologic treatment options for osteoarthritis (OA)?

What is the role of a physiatrist in the treatment of osteoarthritis (OA)?

What is the role of mesenchymal stem cell therapy in the treatment of osteoarthritis (OA)?

Which analgesics are most effective in the treatment of osteoarthritis (OA)?

What are the risks and benefits of acetaminophen for the treatment of osteoarthritis (OA)?

What are the possible adverse effects of NSAIDs for the treatment of osteoarthritis (OA)?

What is the efficacy of topical diclofenac for the treatment of osteoarthritis (OA)?

How do NSAIDs affect blood pressure and kidney function when used for treatment of osteoarthritis (OA)?

What is the initial treatment of mild or moderate osteoarthritic pain?

What is the treatment regimen for osteoarthritis (OA) with intermittent symptoms?

What is the role of topical NSAIDs in the treatment of osteoarthritis (OA)?

What are the treatment options for highly resistant osteoarthritic pain?

Is hydroxychloroquine effective at relieving synovitis in patients with hand osteoarthritis (OA)?

What is the role of duloxetine in the treatment of osteoarthritis (OA)?

What is the role of intra-articular pharmacologic therapy for osteoarthritis (OA)?

What is the role of synovial fluid aspiration in the treatment of osteoarthritis (OA)?

What is the role of steroid injections in the treatment of osteoarthritic knee pain?

What is the role of Zilretta in the treatment of osteoarthritis (OA)?

What is the role of corticosteroid injections in the treatment of osteoarthritis (OA) of the hip?

What are the limitations of steroid injections in the treatment of osteoarthritis (OA)?

What is the role of intra-articular injection of sodium hyaluronate for the treatment of osteoarthritis (OA)?

Which intra-articular hyaluronic acids (HAs) have FDA approval for the treatment of osteoarthritic knee pain?

What are sources of hyaluronic acids (HAs) for the treatment of osteoarthritis (OA)?

Which intra-articular hyaluronic acids (HAs) are safe for repeat treatment of osteoarthritis (OA)?

What is the mechanism of action of hyaluronic acids (HAs) for the treatment of osteoarthritis (OA)?

What are the possible adverse effects of hyaluronic acid (HA) for the treatment of osteoarthritis (OA)?

What is the efficacy of prolotherapy for the treatment of osteoarthritis (OA)?

What is the role of muscle relaxants in the treatment of osteoarthritis (OA)?

What is the role of glucosamine and chondroitin sulfate in the treatment of osteoarthritis (OA)?

What is the role of S-adenosylmethionine (SAM-e) in the treatment of osteoarthritis (OA)?

What is the role of chondroprotective drugs in the treatment of osteoarthritis (OA)?

What is the role of anti- nerve growth factor (NGF) in the treatment of osteoarthritis (OA)?

What is the role of lifestyle modification in the treatment of osteoarthritis (OA)?

What are the short-term and long-term benefits of physical therapy for osteoarthritis (OA)?

Which lifestyle modifications may reduce or relieve pain and stress in patients with osteoarthritis (OA)?

How is exercise beneficial in the treatment of osteoarthritis (OA)?

Why are stretching exercises useful in the treatment of osteoarthritis (OA)?

What is the difference in outcome between non-weight bearing and weight-bearing exercises for the treatment of osteoarthritis
(OA)?

What is the difference in outcome between home-based strength and home-based balance training for the treatment of
osteoarthritis (OA)?

What is the role of aerobic conditioning for the treatment of osteoarthritis (OA)?

How can adherence to home-based exercise treatment be increased in patients with osteoarthritis (OA)?

What is the efficacy of tai chi in the treatment of osteoarthritis (OA)?

What are assistive devices used in the treatment of osteoarthritis (OA)?

What are the ACR conditional recommendations for the use of assistive devices in the treatment of osteoarthritis (OA) of the
hand?

What are the ACR recommendations for use of assistive devices in the treatment of osteoarthritis (OA) of the knee?

What is the role of occupational and physical therapy in the treatment of osteoarthritis (OA)?

What is the role of pulsed electromagnetic field stimulation in the treatment of osteoarthritis (OA)?

What is the role of pulsed short-wave treatment for osteoarthritis (OA)?

What is the efficacy of transcutaneous electrical nerve stimulation (TENS) for the treatment of osteoarthritis (OA)?

What is the efficacy of acupuncture for the treatment of osteoarthritis (OA)?

What are the guidelines for the use of acupuncture to treat osteoarthritis (OA)?

What is the role of arthroscopy in the treatment of osteoarthritis (OA)?

When is arthroscopy indicated for the treatment of osteoarthritis (OA)?

What postoperative therapy is required following treatment of osteoarthritis (OA) with arthroscopy?

What is the indication for osteotomy in the treatment of osteoarthritis (OA)?

What is the efficacy of osteotomy for the treatment of osteoarthritis (OA)?

What are the contraindications for osteotomy for the treatment of osteoarthritis (OA)?

What postoperative therapy is required following osteotomy for the treatment of osteoarthritis (OA)?

What is the role of arthroplasty in the treatment of osteoarthritis (OA)?

What is the indication for arthroplasty in the treatment of osteoarthritis (OA)?

What are possible postoperative complications of arthroplasty for osteoarthritis (OA)?

What postoperative therapy is required following arthroplasty for osteoarthritis (OA)?

What is the role of fusion in the treatment of osteoarthritis (OA)?

What is the role of joint lavage in the treatment of osteoarthritis (OA)?

How is osteoarthritis (OA) prevented?

What is the role of mesenchymal stem cells (MSCs) in the treatment of osteoarthritis (OA)?

How are mesenchymal stem cells (MSCs) harvested for the treatment of osteoarthritis (OA)?

What is the efficacy of mesenchymal stem cell therapy for the treatment of osteoarthritis (OA)?

Guidelines

Which organizations have issued guidelines on the treatment of osteoarthritis (OA)?

What are the ACR treatment recommendations for osteoarthritis (OA) of the hand?

What are the guidelines on nonpharmacologic treatment of knee osteoarthritis (OA)?

What are the AAOS recommendations for lifestyle modifications for the treatment of knee osteoarthritis (OA)?

What are the guideline recommendations on the use of acupuncture for the treatment of knee osteoarthritis (OA)?

What are the ARC recommendations on pharmacotherapy for the treatment of knee osteoarthritis?

What are the AAOS recommendations on pharmacotherapy for the treatment of knee osteoarthritis?

What is the AAOS recommendation on acetaminophen for the treatment of osteoarthritis (OA) of the knee?

What are the AAOS guidelines for total knee arthroplasty in the treatment of osteoarthritis (OA)?

Which treatments of osteoarthritis (OA) of the knee are not recommended by AAOS?

What are the OARSI recommendations for nonpharmacologic treatment of hip osteoarthritis (OA)?

What are the ACR recommendations for nonpharmacologic treatment of hip osteoarthritis (OA)?

What are the ACR recommendations for pharmacologic treatment of osteoarthritis (OA) of the hip?

Which treatments does the ACR recommend against for osteoarthritis (OA) of the hip?

Medications

What are the goals of drug treatment for osteoarthritis (OA)?

Which medications are used in the treatment of osteoarthritis (OA)?

Which medications in the drug class Antirrheumatic, Miscellaneous are used in the treatment of Osteoarthritis?

Which medications in the drug class Corticosteroids are used in the treatment of Osteoarthritis?

Which medications in the drug class Opioid Analgesics are used in the treatment of Osteoarthritis?

Which medications in the drug class Analgesic, Topical are used in the treatment of Osteoarthritis?

Which medications in the drug class Antidepressants, SNRIs are used in the treatment of Osteoarthritis?

Which medications in the drug class Calcium Channel Blocker/COX-2 Inhibitor Combination are used in the treatment of
Osteoarthritis?

Which medications in the drug class Nonsteroidal Anti-inflammatory Drugs (NSAIDs) are used in the treatment of Osteoarthritis?

Which medications in the drug class Analgesics, Other are used in the treatment of Osteoarthritis?

Which medications in the drug class Skeletal muscle relaxants are used in the treatment of Osteoarthritis?

 
Contributor Information and Disclosures

Author

Carlos J Lozada, MD Director of Rheumatology Fellowship Training Program, Professor of Clinical Medicine, Department of
Medicine, Division of Rheumatology and Immunology, University of Miami, Leonard M Miller School of Medicine

Carlos J Lozada, MD is a member of the following medical societies: American College of Physicians, American College of
Rheumatology

Disclosure: Received honoraria from Pfizer for consulting; Received grant/research funds from AbbVie for other; Received
honoraria from Heel for consulting.

Coauthor(s)

Schartess S Culpepper Pace, MD Assistant Professor of Medicine, Division of Rheumatology, University of Miami, Leonard M
Miller School of Medicine

Schartess S Culpepper Pace, MD is a member of the following medical societies: American College of Rheumatology

Disclosure: Nothing to disclose.

Chief Editor

Herbert S Diamond, MD Visiting Professor of Medicine, Division of Rheumatology, State University of New York Downstate
Medical Center; Chairman Emeritus, Department of Internal Medicine, Western Pennsylvania Hospital

Herbert S Diamond, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians,
American College of Rheumatology, American Medical Association, Phi Beta Kappa

Disclosure: Nothing to disclose.

Acknowledgements

Samuel Agnew, MD, FACS Associate Professor, Departments of Orthopedic Surgery and Surgery, Chief of Orthopedic Trauma,
University of Florida at Jacksonville College of Medicine; Consulting Surgeon, Department of Orthopedic Surgery, McLeod
Regional Medical Center

Samuel Agnew, MD, FACS is a member of the following medical societies: American Association for the Surgery of Trauma,
American College of Surgeons, Orthopaedic Trauma Association, and Southern Orthopaedic Association

Disclosure: Nothing to disclose.

Elliot Goldberg, MD Dean of the Western Pennsylvania Clinical Campus, Professor, Department of Medicine, Temple University
School of Medicine

Elliot Goldberg, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, and
American College of Rheumatology

Disclosure: Nothing to disclose.

Siriporn Janchai, MD Fellow, Department of Medicine, Section of Physical Medicine and Rehabilitation, Louisiana State University
Health Science Center

Disclosure: Nothing to disclose.

James Monroe Laborde, MD, MS Clinical Assistant Professor, Department of Orthopedics, Louisiana State University Health
Sciences Center and Tulane Medical School; Adjunct Assistant Professor, Department of Biomedical Engineering, Tulane
University; Adjunct Assistant Professor, Department of Physical Medicine and Rehabilitation, Louisiana State University Medical
School

James Monroe Laborde, MD, MS is a member of the following medical societies: American Academy of Orthopaedic Surgeons

Disclosure: Nothing to disclose.

Phillip J Marone, MD, MSPH Clinical Professor, Department of Orthopedic Surgery, Jefferson Medical College
Phillip J Marone, MD, MSPH is a member of the following medical societies: American Academy of Orthopaedic Surgeons,
American College of Surgeons, American Medical Association, American Orthopaedic Society for Sports Medicine, and
Philadelphia County Medical Society

Disclosure: Nothing to disclose.

Furqan H Siddiqui, MD Assistant Professor of Medicine (Research), Louisiana State University Medical Center in New Orleans

Disclosure: Nothing to disclose.

Eli Steigelfest, MD Consulting Staff, Department of Rheumatology, The Consultant Group, PC

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy;
Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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